OROncology Reports1021-335X1791-2431D.A. Spandidos10.3892/or.2025.8893OR-53-5-08893ReviewRoles of PEG10 in cancer and neurodegenerative disorder (Review)MouDachao12*WuShasha12*ChenYanqiong12*WangYun12DaiYufang12TangMin34TengXiu12BaiShijun5BaiXiufeng12Laboratory of Human Disease and Immunotherapies, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. ChinaInstitute of Inflammation and Immunology (I3), Frontiers Science Center for Disease-Related Molecular Network, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. ChinaDivision of Thoracic Tumor Multimodality Treatment and Department of Radiation Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. ChinaLaboratory of Clinical Cell Therapy, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. ChinaDepartment of Agriculture Forestry and Food Engineering, Yibin University, Lingang Economic and Technological Development Zone, Yibin, Sichuan 644000, P.R. ChinaCorrespondence to: Professor Xiufeng Bai, Laboratory of Human Disease and Immunotherapies, West China Hospital, Sichuan University, Building B2, 88 Keyuan South Road, Wuhou, Chengdu, Sichuan 610041, P.R. China, E-mail: baixiufeng@wchscu.cn Professor Shijun Bai, Department of Agriculture Forestry and Food Engineering, Yibin University, Lingang Economic and Technological Development Zone, 5, 3rd Section of Daxuecheng Road, Yibin, Sichuan 644000, P.R. China, E-mail: bsj11@126.com
Paternally expressed gene 10 (PEG10) is an imprinting gene. In addition to its known roles in placental development, as well as mouse embryonic stem cell and trophoblast stem cell differentiation, PEG10 has recently been shown to have significance in cancers. High expression of PEG10 is observed in various cancer types and is associated with poor prognosis. Of note, disruption of PEG10 expression leads to increased apoptosis, as well as decreased proliferation, invasion and migration of cancer cells. PEG10 is expected to become a target for cancer and neurodegenerative disorder therapy. This article reviewed the latest progress in the role of PEG10 in cancers.
PEG10cancerneurodegenerative disorderNational Science Foundation of Sichuan Province2023NSFSC1555National Clinical Research Center for Geriatrics, West China Hospital, Sichuan UniversityZ20192008special fund in West China Hospital, Sichuan University0084204150311·3·5 project for disciplines of excellence, West China Hospital, Sichuan UniversityZYJC18003This work was supported by the National Science Foundation of Sichuan Province (grant no. 2023NSFSC1555), the National Clinical Research Center for Geriatrics, West China Hospital, Sichuan University (grant no. Z20192008), the special fund in West China Hospital, Sichuan University (grant no. 008420415031) and the 1·3·5 project for disciplines of excellence, West China Hospital, Sichuan University (grant no. ZYJC18003).Introduction
In tumors, certain genes related to proliferation and invasion are upregulated in expression (1). In neurodegenerative diseases, there are also a bulk of genes with abnormal expression, including genes related to the autophagy-lysosomal pathway (2). These abnormally expressed genes may not only serve as biomarkers for disease diagnosis, but also as targets for treatment. Human endogenous retroviruses (HERVs) are derived from ancient retroviruses, which infect and insert viral genes into germline cells. HERVs constitute an estimated 8% of the human genome (3). In general, a complete HERV includes 5′ long terminal repeats (5′ LTR), a primer-binding site, group-specific antigen gene (gag), a protease gene, a polymerase gene (pol), an envelope gene and 3′ LTR elements (4). Paternally expressed imprinted gene 10 (PEG10) is an evolutionarily conserved HERV gene (5) belonging to the Ty3/Gypsy family of retrotransposons. Evolutionarily, PEG10 is a therian-specific gene (6,7), and differentially methylated regions of PEG10 have emerged in the therian ancestor at least 160 million years ago (8). During the evolution of the placenta in mammals, PEG10 was inserted into the genome, as it exists in marsupials but not in egg-laying monotreme species (9). PEG10 is a paternally expressed imprinting gene, which was reported to be located at human chromosome 7q21 in 2001 for the first time (7). Importantly, PEG10 can be used for RNA delivery (10–13). As an imprinting gene, PEG10 is crucial for placental development and plays a key role in mouse embryonic stem cell and trophoblast stem cell differentiation (14–16). Ono et al (17) have reported that PEG10 maintains placental function, and deletion of PEG10 in mice can lead to embryonic lethality. Traditionally, PEG10 expression is limited to the testes, adrenal gland and skin after adulthood (18). During the past few years, knowledge of PEG10 being highly expressed in tumors and neurodegenerative diseases has emerged. Thus, the present article reviewed the recent findings on the roles of PEG10 in these diseases.
The structural domains of the PEG10 protein
PEG10 contains 2 overlapping open reading frames (RF1 and RF1/2), and the mRNA of PEG10 utilizes a typical retroviral frameshift mechanism to encode two proteins: RF1 (encoding gag-like protein) and RF1/2 (encoding gag-pol-like polyprotein) (19,20). The frameshifting efficiency of PEG10 is ~22% (19) and a study has identified that the frameshift of PEG10 can be suppressed by a small-molecule compound (21). The ribosomal frameshift element of PEG10 consists of ‘slippery’ and ‘pseudoknot’. The slippery sequence is GGGAAAC, while pseudoknot is composed of multiple stem-loop structures. When ribosomes encounter the pseudoknot, the A- and P-site tRNAs detach from the zero frame codons GGA-AAC, shifting back one nucleotide to GGG-AAA, causing the original encoding of glycine-asparagine to change to glycine-lysine (22). PEG10 has multiple evolutionary conserved functional domains, including a coiled-coil domain, retrotransposon-gag domain, retrovirus zinc finger-like domain, retroviral asparytyl protease domain and reverse transcriptase domain (5,7,23–26). The structure of PEG10 is shown in Fig. 1.
PEG10 as a long non-coding (lnc)RNA
LncRNA is a type of ncRNA with a length exceeding 200 nucleotides. LncRNAs are involved in the occurrence, development and progression of cancer. PEG10 is an upregulated lncRNA in patients with lymphoma (27). In diffuse large B-cell lymphoma (DLBCL), lncRNA PEG10 inhibits microRNA (miR)-101-3p, while miR-101-3p inhibits kinesin family member 2A (KIF2A). Therefore, overexpression of PEG10 leads to an increase in KIF2A expression, promoting DLBCL growth (28,29). LncRNA PEG10 inhibits miR-449a, increases ribosomal protein S2 expression and increases the proliferation, invasion and migration of neuroblastoma cells (30). LncRNA PEG10 and H19 are mutual upstream and downstream regulatory factors, and PEG10 levels are constitutively associated with a high lymph node ratio in gastric cancer (31). Furthermore, knockout of PEG10 causes an increase in miR-3200 and inhibits the proliferation, migration and invasion of gastric cancer cells (32) and glioma cells (33). LncRNA PEG10 inhibits miR-33a in melanoma, thus inhibiting the PI3K/AKT and mTOR pathways (34). Furthermore, overexpression of lncRNA PEG10 also has an essential role in promoting proliferation and invasion in esophageal cancer cells (35) and hypopharyngeal squamous cell carcinoma (36).
PEG10 subcellular localization
PEG10 contains 2 overlapping open reading frames, RF1 and RF2. During embryonic development, PEG10-RF1 and PEG10-RF1/2 proteins are expressed at different stages, suggesting that PEG10-RF1 and PEG10-RF1/2 may have different functions. PEG10-RF1/2 have an aspartate protease domain and new fragments can be generated through self-cutting (19,22). PEG10 is found in multiple cellular components, including the nucleus (24), extracellular vesicles and stress granules (25). PEG10-RF1 has nuclear and cytoplasmic localization and does not enter stress granules under stress conditions. However, PEG10-RF1/2 is only localized in the cytoplasm and enters stress granules under stress conditions (25). PEG10-RF1 contains a retroviral zinc finger domain and is considered a transcription factor, regulates the transcription of genes participates in the progression of cancers and neurodegenerative diseases; these genes include C9orf72-SMCR8 complex subunit, doublecortin like kinase 1, plexin A4, semaphorin 5B, slit guidance ligand 3 and Wnt family member 3A (24).
In addition, PEG10 is a secreted protein produced by Dental-derived mesenchymal stem cells and bone marrow stem cells, which is associated with adipose differentiation. PEG10 expression is generally observed at the immediate early stage of adipocyte differentiation (37).
Mechanisms leading to PEG10 activation and inactivation
The increase in PEG10 protein may be caused by various ways, including DNA demethylation, gene duplication, extended RNA half-life, transcriptional activation and inhibition of protein degradation (Fig. 2).
Epigenetic regulation
In the mammalian genome, DNA methylation is an important approach to govern gene expression (38,39). DNA methylation usually inhibits gene expression by recruiting repression proteins or inhibiting transcription factors to DNA. In human parthenogenetic embryonic stem cells, activating transcription factor 7 interacting protein increases PEG10 methylation and inhibits its transcription (40). In KrasG12D-induced T-cell neoplasms, imprinting control regions (ICRs) of PEG10 are significantly hypermethylated. Increased DNA methylation at the ICRs of PEG10 is the earliest detectable change in lymphocytic T-cell thymic lymphoma (41). Tet methylcytosine dioxygenase 1 (TET1) is a maintenance DNA demethylase, which promotes PEG10 expression by inhibiting DNA methylation, and deleting TET1 results in an increase of 5-hydroxymethylcytosine in PEG10, leading to a decrease in PEG10 expression (42). Histone methylation is another way to regulate PEG10 expression, and in hepatocellular carcinoma (HCC), menin/mixed-lineage leukemia 1 (MLL) interaction inhibitor MI-503 prevents the display of the menin-MLL1 complex from binding to the PEG10 promoter, reduces the modification of trimethylated H3 lysine 4 in the promoter region and inhibits PEG10 transcription (43).
Gene amplification
Traditionally, gene amplification was identified as one aspect of the genetic instability strongly associated with malignantly transformed cells. Cancer cells use this mechanism to mediate overexpression of certain oncogenes to promote proliferation, anti-apoptosis and resistance to anticancer drugs (44). For instance, genomic amplification of PEG10 at the 7q21.3 locus was found in HCC samples (45,46). In hepatitis B virus-associated HCC, the increase in DNA copy number leads to an increased expression of PEG10 (47).
RNA stability
The stability of mRNA plays an important role in the control of gene expression (48). PEG10 is a direct target of miRNA-574-5p (30). MiR-138-5p binds to the 3′UTR of PEG10 mRNA, shortening the half-life of PEG10 mRNA (49). In regulating retinoblastoma (RB), the circular RNA Circ:0075804 promotes PEG10 expression by inhibiting miR-138-5p (49). N6-methyladenosine residues on the PEG10 3′UTR are recognized and bind by insulin like growth factor 2 mRNA binding protein 1 to recruit poly (A) Binding Protein Cytoplasmic 1 and enhance the stability of PEG10 mRNA, thereby increasing the protein content of PEG10 (50). In neural progenitor cells, TET3 increases the DNA methylation levels of PEG10 and maintains neural stem cell identity (51). In HCC, miR-122 binds to the PEG10 3′UTR and inhibits PEG10 expression (52). LncRNA SNAI3 antisense RNA 1 increases PEG10 expression through competing endogenous RNA spreading of miR-27a-3p and miR-34a-5p, thereby promoting cancer cell proliferation (53). In human colon cancer cells, miR-491 binds to the 3′UTR of PEG10 mRNA and inhibits PEG10 expression (54). In colorectal cancer, NOTCH1-associated lncRNA in T-cell acute lymphoblastic leukemia 1 increases PEG10 expression to promote tumor progression by sponging miR-574-5p (55).
Transcriptional regulation
Transcription factors can bind to the promoter region of PEG10 and activate its transcription. Myc promotes tumor-cell proliferation by activating PEG10 transcription (56,57). In addition, the E2F family of transcription factors (E2Fs) are transcription factors that promote the transcription of PEG10 and thereby enhance the proliferation of HCC cells (58). Glycogen synthase kinase 3β can phosphorylate and activate E2F transcriptional factor 1 (E2F1). Phosphorylated E2F1 binds to ubiquitin specific peptidase 11, leading to reduced degradation of E2F1 due to deubiquitination. E2F-1 has also been recently shown to be crucial for PEG10 activation in pancreatic cancer, and to further promote cell proliferation, migration and invasion (59). Similarly, in HCC, the expression of PEG10 is positively correlated with lymph node metastasis. Overexpression of PEG10 promotes epithelial-mesenchymal transition, and the expression of PEG10 is influenced by the transforming growth factor β (TGF-β) signaling (60). Furthermore, transcription factor CTR9 homolog, Paf1/RNA polymerase II complex component promotes PEG10 transcription (61).
Although TGF-β promotes PEG10 expression in HCC tissues, in other cancer tissues, the expression of PEG10 is inhibited by TGF-β, e.g. in chondrosarcoma cells (62). Furthermore, the upregulated PEG10 activity in turn inhibits TGF-β and bone morphogenetic protein signaling (63). The transcription factor one cut homeobox 2 binds to the PEG10 promoter and increases the mRNA levels of PEG10 in lethal prostate cancer (64,65), and recent studies demonstrated that androgen receptor (AR) inhibits the transcription of PEG10 (66–68). RB inhibits PEG10 transcription by inhibiting E2F1 activity (26,58). Interestingly, the expression of PEG10 can be regulated by small molecule compounds. For instance, curcumin inhibits the expression of PEG10 in an unknown mechanism, thereby inhibiting the growth of breast cancer cells (69). Exposure to cadmium (Cd) can cause a decrease in the expression of Cd-exposed placentas PEG10 (70).
Protein stability
PEG10 has a C-terminal polyproline repeat domain, which may be recognized by human ubiquilin 2 (UBQLN2) and facilitates its proteasomal degradation (24,71). The deficiency of UBQLN2 leads to an increase in PEG10 protein. Furthermore, the ubiquitin protein ligase E3A (UBE3A) is another PEG10 regulating gene. UBE3A inhibits the expression of PEG10 via the proteasome (25)
Downstream of PEG10
Nuclear localized PEG10 functions as a transcription factor, mediating the transcription of numerous downstream target genes. Kruppel-like factor 2 (KLF2) is an inhibitory factor of NF-κB and PEG10 activates NF-κB signaling by inhibiting KLF2 expression (23). Upregulated PEG10 expression activates NOTCH signaling and promotes metastatic cancer stem cell self-renewal (72). PEG10 was reported to bind to TGF-β receptor ALK1 and to inhibit ALK1 as well as ALK5 signaling (73). In HCC, TSG101 binds to PEG10 to prevent its degradation, thereby enhancing PEG10 expression and downstream target genes p53, p21 and matrix metalloproteinases (MMPs), leading to cell proliferation, invasion and migration (74). After overexpression of PEG10 in human colon cancer cells, the Wnt1/β-catenin pathway is activated, promoting cell proliferation and inhibiting cell apoptosis (54). In Burkitt's lymphoma cells, PEG10 promotes tumor cell invasion and metastasis by upregulating the expression of MMP-2 and −9 (18,26,59,75). PEG10 promotes the proliferation of endometrial cancer cells by inhibiting the transcription of p16 and p18 genes. PEG10 tends to bind to the TGGGAYTACA and CTCNGCCTCC motifs (50). Of note, it was recently found that PEG10 is an RNA binding protein, promoting trophoblast stem cell differentiation into placental lineages (14).
PEG10 in cancer
PEG10 is considered an oncogene and PEG10 protein has been found to be significantly increased in various cancer types to date. Exogenous PEG10 expression leads to increased cellular proliferation and increased cell viability (76).
Liver cancer
The relationship between PEG10 and cancer was first studied in liver cancer. PEG10 is strongly expressed in HCC (77). A machine learning study found that PEG10 is highly expressed in patients unresponsive to transarterial chemotherapy (78). Expression of PEG10 is significantly correlated with poor survival and tumor recurrence in HCC, making PEG10 an independent predictor of early recurrence of HCC (79). However, other studies found that PEG10 has an inhibitory effect on tumor cell growth by activating immune response. For instance, transduction of dendritic cells with PEG10 recombinant adenovirus induced anti-tumor immunity against HCC (80). Another study also identified that androgens activate PEG10 (81). Thereby, PEG10 is the potential biomarker of HCC (82,83).
Lung cancer
An increase in PEG10 content is closely related to the prognosis of lung cancer; therefore, PEG10 is a diagnostic and prognostic gene for lung adenocarcinoma and squamous cell carcinoma (84). E2Fs activate MMPs by upregulating PEG10, leading to lung cancer progression, prognosis and metastasis (85,86). E2F1 activates PEG10 gene transcription, promoting proliferation of lung epithelial cells (87). Furthermore, transcription termination factor 1 activates receptor tyrosine kinase like orphan receptor 1 (ROR1), which activates PEG10 transcription. Inhibition of ROR1 by small inhibitory (si)RNA in the human lung cancer cell line PC-9 leads to a decrease in the transcription level of PEG10 (88). On the contrary, the expression of PEG10 is also inhibited by certain transcription factors. The expression of PEG10 is inhibited by PI3K/AKT, which leads to a decrease in PEG10 protein levels in lung cancer cells (89).
Prostate cancer
The expression of PEG10 in prostate cancer is usually suppressed, as AR inhibits the transcription of PEG10 (26). However, during the treatment of prostate cancer, AR inhibitors drive cancer cells to evolve into neuroendocrine prostate cancer (NEPC) and the expression of PEG10 gradually increases during the transition from adenocarcinoma to NEPC. Therefore, PEG10 can be used as a predictive indicator for biochemical recurrence of prostate cancer (90). As a characteristic gene of NEPC, silencing PEG10 inhibits the in vitro growth of prostate cancer cells (91). In AR activated adenocarcinoma type prostate cancer, full-length RF1/2 is the dominant form, while in NEPC cells, RF1 and RF1/2 are both highly expressed (26). Full-length PEG10 (RF1/2) drive the proliferation of NEPC, while short-length PEG10 (RF1) promotes invasion (26). The expression of PEG10 is associated with short survival of patients with prostate adenocarcinoma (92). Importantly, studies have highlighted the crucial role of PEG10 in promoting the malignant transformation of the highly lethal AR-negative phenotype prostate cancer (93). Silencing PEG10 reduced the expression of neuroendocrine markers and inhibited cell proliferation (94).
Leukemia
Driven by genomic gains and promoter demethylation, PEG10 is highly expressed and is associated with poor patient prognosis in mycosis fungoides-large-cell transformation (23). Furthermore, PEG10 overexpression was observed in B-cell acute lymphoblastic leukemia and B-cell chronic lymphocytic leukemia (95,96). Reducing PEG10 expression leads to a decrease in cell volume and a weakened colony-formation ability in large transformed cutaneous T-cell lymphoma cells; consequently, PEG10 inhibition may be a promising treatment for advanced invasive T-cell lymphoma (23). In thymoma, the DNA methylation level of the promoter region of PEG10 is higher than that of T-cell lymphoblastic leukemia (97,98). Abnormal DNA methylation in PEG10 ICRs is expected to become a prognostic marker for T-cell neoplasm and B-cell chronic lymphocytic leukemia (41,99).
Other cancer types
To date, PEG10 has been shown to be crucial in several types of cancer, such as Ewing sarcoma (ES), esophageal squamous cell carcinoma (ESCC) and metastatic thymic adenocarcinoma. In ES, PEG10 inhibits the TGF-β pathway and reduces cell growth. In the human skin epidermoid carcinoma cell line A431, miR-145, miR-432 and miR-1972 inhibit PEG10 expression (100). Besides, genetic mutations can also affect PEG10 activity. In metastatic thymic adenocarcinoma, PEG10 was found to have a somatic p.R207H mutation (101). LncRNA PEG10 is elevated in serum exosomes of patients with ESCC (102). Higher PEG10 levels are associated with unfavorable overall and progression-free survival (103). Therefore, PEG10 can serve as a marker of carcinogenesis, progression and poor prognosis, as well as a putative drug target in ovarian cancer (72,104,105), rectal adenocarcinoma (106), early-onset colorectal cancer (107), neuroendocrine muscle-invasive bladder cancer (108), bladder cancer (108), adenosquamous carcinomas (109), gallbladder adenocarcinoma (110), breast cancer (111,112), adenocarcinoma (113), oral squamous cell carcinoma (114) and glioma (115).
ALS is a chronic neurodegenerative disease that mainly causes damage to upper and lower motor neurons. Mutations in the ubiquitin-adaptor protein UBQLN2 is considered one of the causes of ALS (116,117). PEG10 is a substrate of UBQLN2 (118); UBQLN2 binds to the C-terminus of PEG10 and initiates its degradation (24).
Angelman syndrome
Angelman syndrome is caused by UBE3A defect; patients with Angelman syndrome often experience developmental delay, balance disorders, limb incoordination and gait instability. The UBE3A mutation causes PEG10 aggregation, alters neuronal migration and ultimately leads to Angelman syndrome (25).
Therapeutic strategies to target PEG10-driven diseases
Although no targeted small-molecule inhibitors to block PEG10 have been developed, there are still numerous ways to inhibit PEG10, including inhibitors that target its transcription factors, siRNAs, shRNAs or miRNAs that target PEG10 mRNA, as well as using PEG10 as an antigen to develop vaccines (119). PEG10-related treatment methods are listed in Table I. The functional diversity of PEG10 poses multiple challenges to drug development, and ensuring target specificity is key in drug development to avoid unnecessary damage to embryo development or normal tissue function.
Conclusions
PEG10 can be used for RNA delivery (10). PEG10 is an imprinting gene expressed in the placenta and tumors. Silencing PEG10 expression in cancer cells slows cell growth, increases apoptosis, and reduces invasion and metastasis. PEG10 is a promising therapeutic target and prognostic marker for cancer. However, due to its nuclear distribution, PEG10 is not suitable for antibody drug development. Synthetic PEG10 siRNA is a potential therapeutic agent. In addition, small molecules targeting the ribosomal frameshift of PEG10 are a promising approach (120,121).
Acknowledgements
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Availability of data and materials
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Authors' contributions
DM, SB and XB were involved in the conceptualization of the study. SW and YC wrote the original draft. YW and YD prepared the figures. MT and XT reviewed and revised the manuscript. All authors reviewed the manuscript and have read and approved the final version. Data authentication is not applicable.
Ethics approval and consent to participate
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Patient consent for publication
Not applicable.
Competing interests
The authors declare that they have no competing interests.
ReferencesHanahanDHallmarks of cancer: New dimensionsCancer Discov123146202210.1158/2159-8290.CD-21-105935022204LeeMSKimJWParkDGHeoHKimJYoonJHChangJAutophagic signatures in peripheral blood mononuclear cells from Parkinson's disease patientsMol Cells48100173202410.1016/j.mocell.2024.10017339730076DopkinsNNixonDFActivation of human endogenous retroviruses and its physiological consequencesNat Rev Mol Cell Biol25212222202410.1038/s41580-023-00674-z37872387JakobssonJVincendeauMSnapShot: Human endogenous retrovirusesCell185400400.e1202210.1016/j.cell.2021.12.02835063077YoungsonNAKocialkowskiSPeelNFerguson-SmithACA small family of sushi-class retrotransposon-derived genes in mammals and their relation to genomic imprintingJ Mol Evol61481490200510.1007/s00239-004-0332-016155747IwasakiSSuzukiSPelekanosMClarkHOnoRShawGRenfreeMBKaneko-IshinoTIshinoFIdentification of a novel PNMA-MS1 gene in marsupials suggests the LTR retrotransposon-derived PNMA genes evolved differently in marsupials and eutheriansDNA Res20425436201310.1093/dnares/dst02023704700OnoRKobayashiSWagatsumaHAisakaKKohdaTKaneko-IshinoTIshinoFA retrotransposon-derived gene, PEG10, is a novel imprinted gene located on human chromosome 7q21Genomics73232237200110.1006/geno.2001.649411318613RenfreeMBSuzukiSKaneko-IshinoTThe origin and evolution of genomic imprinting and viviparity in mammalsPhilos Trans R Soc Lond B Biol Sci36820120151201310.1098/rstb.2012.015123166401SuzukiSOnoRNaritaTPaskAJShawGWangCKohdaTAlsopAEMarshall GravesJAKoharaYRetrotransposon silencing by DNA methylation can drive mammalian genomic imprintingPLoS Genet3e55200710.1371/journal.pgen.003005517432937SegelMLashBSongJLadhaALiuCCJinXMekhedovSLMacraeRKKooninEVZhangFMammalian retrovirus-like protein PEG10 packages its own mRNA and can be pseudotyped for mRNA deliveryScience373882889202110.1126/science.abg615534413232TangRGuoLWeiTChenTYangHYeHLinFZengYYuHCaiZLiuXEngineering PEG10 assembled endogenous virus-like particles with genetically encoded neoantigen peptides for cancer vaccinationElife13RP98579202410.7554/eLife.98579.339269893CampodonicoWMohanHMHuynhPTBlackHHLauCIPaulsonHLSharkeyLMWhiteleyAMThe gag-like gene RTL8 antagonizes PEG10-mediated virus like particlesPLoS One19e0310946202410.1371/journal.pone.031094639775359LiMLiuZWangDYeJShiZPanCZhangQJuRZhengYLiuYIntraocular mRNA delivery with endogenous MmPEG10-based virus-like particlesExp Eye Res243109899202410.1016/j.exer.2024.10989938636802AbedMVerschuerenEBudayevaHLiuPKirkpatrickDSRejaRKummerfeldSKWebsterJDGierkeSReicheltMThe Gag protein PEG10 binds to RNA and regulates trophoblast stem cell lineage specificationPLoS One14e0214110201910.1371/journal.pone.021411030951545PollardKSSerreDWangXTaoHGrundbergEHudsonTJClarkAGFrazerKA genome-wide approach to identifying novel-imprinted genesHum Genet122625634200810.1007/s00439-007-0440-117955261SmallwoodAPapageorghiouANicolaidesKAlleyMKJimANargundGOjhaKCampbellSBanerjeeSTemporal regulation of the expression of syncytin (HERV-W), maternally imprinted PEG10, and SGCE in human placentaBiol Reprod69286293200310.1095/biolreprod.102.01307812620933OnoRNakamuraKInoueKNaruseMUsamiTWakisaka-SaitoNHinoTSuzuki-MigishimaROgonukiNMikiHDeletion of Peg10, an imprinted gene acquired from a retrotransposon, causes early embryonic lethalityNat Genet38101106200610.1038/ng169916341224XieTPanSZhengHLuoZTemboKMJamalMYuZYuYXiaJYinQPEG10 as an oncogene: Expression regulatory mechanisms and role in tumor progressionCancer Cell Inte18112201810.1186/s12935-018-0610-330123090ClarkMBJänickeMGottesbührenUKleffmannTLeggeMPooleESTateWPMammalian gene PEG10 expresses two reading frames by high efficiency-1 frameshifting in embryonic-associated tissuesJ Biol Chem2823735937369200710.1074/jbc.M70567620017942406ManktelowEShigemotoKBrierleyICharacterization of the frameshift signal of Edr, a mammalian example of programmed-1 ribosomal frameshiftingNucleic Acids Res3315531563200510.1093/nar/gki29915767280CardnoTSShimakiYSleebsBELackovicKParisotJPMossRMCrowe-McAuliffeCMathewSFEdgarCDKleffmannTTateWPHIV-1 and human PEG10 frameshift elements are functionally distinct and distinguished by novel small molecule modulatorsPLoS One10e0139036201510.1371/journal.pone.013903626447468LuxHFlammannHHafnerMLuxAGenetic and molecular analyses of PEG10 reveal new aspects of genomic organization, transcription and translationPLoS One5e8686201010.1371/journal.pone.000868620084274LiuFGaoYXuBXiongSYiSSunJChenZLiuXLiYLinYPEG10 amplification at 7q21.3 potentiates large-cell transformation in cutaneous T-cell lymphomaBlood139554571202210.1182/blood.202101209134582557BlackHHHansonJLRobertsJELeslieSNCampodonicoWEbmeierCCHollingGATayJWMatthewsAMUngEUBQLN2 restrains the domesticated retrotransposon PEG10 to maintain neuronal health in ALSElife12e79452202310.7554/eLife.7945236951542PandyaNJWangCCostaVLopattaPMeierSZampetaFIPuntAMMientjesEGrossenPDistlerTSecreted retrovirus-like GAG-domain-containing protein PEG10 is regulated by UBE3A and is involved in Angelman syndrome pathophysiologyCell Rep Med2100360202110.1016/j.xcrm.2021.10036034467244AkamatsuSWyattAWLinDLysakowskiSZhangFKimSTseCWangKMoFHaegertAThe placental gene PEG10 promotes progression of neuroendocrine prostate cancerCell Rep12922936201510.1016/j.celrep.2015.07.01226235627YangJWangXRole of long non-coding RNAs in lymphoma: A systematic review and clinical perspectivesCrit Rev Oncol Hematol1411322201910.1016/j.critrevonc.2019.05.00731202125ZhaoJSuLJiangJLong Non-coding RNA paternally expressed imprinted gene 10 (PEG10) elevates diffuse large B-Cell lymphoma progression by regulating kinesin family member 2A (KIF2A) via targeting MiR-101-3pMed Sci Monit26e922810202010.12659/MSM.92281032976381PengWFanHWuGWuJFengJUpregulation of long noncoding RNA PEG10 associates with poor prognosis in diffuse large B cell lymphoma with facilitating tumorigenicityClin Exp Med16177182201610.1007/s10238-015-0350-925864113ZhangJLiuWJiPZhangYSilencing of long chain noncoding RNA paternally expressed gene (PEG10) inhibits the progression of neuroblastoma by regulating microRNA-449a (miR-449a)/ribosomal protein S2 (RPS2) axisBioengineered1363096322202210.1080/21655979.2022.204299935212607IshiiSYamashitaKHaradaHUshikuHTanakaTNishizawaNYokoiKWashioMEmaAMienoHThe H19-PEG10/IGF2BP3 axis promotes gastric cancer progression in patients with high lymph node ratiosOncotarget87456774581201710.18632/oncotarget.2020929088808WangJChuXQZhangDKongDFKnockdown of long non-coding RNA PEG10 inhibits growth, migration and invasion of gastric carcinoma cells via up-regulating miR-3200Neoplasma65769778201810.4149/neo_2018_171204N79429940767XiaoHDingNLiaoHYaoZChengXZhangJZhaoMPrediction of relapse and prognosis by expression levels of long noncoding RNA PEG10 in glioma patientsMedicine (Baltimore)98e17583201910.1097/MD.000000000001758331702614FuYBiYWangFChenXLiuHDeclination of long noncoding RNA paternally expressed gene 10 inhibits A375 cells proliferation, migration, and invasion via mediating microRNA-33aJ Cell Biochem1201986819877201910.1002/jcb.2929231318088ZangWWangTHuangJLiMWangYDuYChenXZhaoGLong noncoding RNA PEG10 regulates proliferation and invasion of esophageal cancer cellsCancer Gene Ther22138144201510.1038/cgt.2014.7725591808ZhaoMSunDLiXXuYZhangHQinYXiaMOverexpression of long noncoding RNA PEG10 promotes proliferation, invasion and metastasis of hypopharyngeal squamous cell carcinomaOncol Lett1429192925201710.3892/ol.2017.649828928830KumarAKumarVRattanVJhaVBhattacharyyaSSecretome proteins regulate comparative osteogenic and adipogenic potential in bone marrow and dental stem cellsBiochimie155129139201810.1016/j.biochi.2018.10.01430367923JungSLeeJSSingle-cell genomics for investigating pathogenesis of inflammatory diseasesMol Cells46120129202310.14348/molcells.2023.000236859476WuYLLinZJLiCCLinXShanSKGuoBZhengMHLiFYuanLQLiZHEpigenetic regulation in metabolic diseases: Mechanisms and advances in clinical studySignal Transduct Target Ther898202310.1038/s41392-023-01333-736864020BarSVershkovDKeshetGLezmiEMellerNYilmazAYanukaONissim-RafiniaMMeshorerEEldar-GevaTBenvenistyNIdentifying regulators of parental imprinting by CRISPR/Cas9 screening in haploid human embryonic stem cellsNat Commun126718202110.1038/s41467-021-26949-734795250BretzCLLangohrIMLeeSKimJEpigenetic instability at imprinting control regions in a Kras(G12D)-induced T-cell neoplasmEpigenetics1011111120201510.1080/15592294.2015.111067226507119YamaguchiSShenLLiuYSendlerDZhangYRole of Tet1 in erasure of genomic imprintingNature504460464201310.1038/nature1280524291790KempinskaKMalikBBorkinDKlossowskiSShuklaSMiaoHWangJCierpickiTGrembeckaJPharmacologic inhibition of the Menin-MLL interaction leads to transcriptional repression of PEG10 and blocks hepatocellular carcinomaMol Cancer Ther172638201810.1158/1535-7163.MCT-17-058029142068ShoshaniOBrunnerSFYaegerRLyPNechemia-ArbelyYKimDHFangRCastillonGAYuMLiJSZChromothripsis drives the evolution of gene amplification in cancerNature591137141202110.1038/s41586-020-03064-z33361815DongHZhangHLiangJYanHChenYShenYKongYWangSZhaoGJinWDigital karyotyping reveals probable target genes at 7q21.3 locus in hepatocellular carcinomaBMC Med Genomics460201110.1186/1755-8794-4-6021767414TsujiKYasuiKGenYEndoMDohiOZenKMitsuyoshiHMinamiMItohYTaniwakiMTanakaSPEG10 is a probable target for the amplification at 7q21 detected in hepatocellular carcinomaCancer Genet Cytogenet198118125201010.1016/j.cancergencyto.2010.01.00420362226HuangJShengHHShenTHuYJXiaoHSZhangQZhangQHHanZGCorrelation between genomic DNA copy number alterations and transcriptional expression in hepatitis B virus-associated hepatocellular carcinomaFEBS Lett58035713581200610.1016/j.febslet.2006.05.03216750200KwonHCBaeYLeeSVThe role of mRNA quality control in the aging of caenorhabditis elegansMole Cells46664671202310.14348/molcells.2023.010337968980ZhangYDouXKongQLiYZhouXCirc_0075804 promotes the malignant behaviors of retinoblastoma cells by binding to miR-138-5p to induce PEG10 expressionInt Ophthalmol42509523202210.1007/s10792-021-02067-734633608ZhangLWanYZhangZJiangYGuZMaXNieSYangJLangJChengWZhuLIGF2BP1 overexpression stabilizes PEG10 mRNA in an m6A-dependent manner and promotes endometrial cancer progressionTheranostics1111001114202110.7150/thno.4934533391523SantiagoMAntunesCGuedesMIacovinoMKybaMReikWSousaNPintoLBrancoMRMarquesCJTet3 regulates cellular identity and DNA methylation in neural progenitor cellsCell Mol Life Sci7728712883202010.1007/s00018-019-03335-731646359ShyuYCLeeTLLuMJChenJRChienRNChenHYLinJFTsouAPChenYHHsiehCWHuangTSmiR-122-mediated translational repression of PEG10 and its suppression in human hepatocellular carcinomaJ Transl Med14200201610.1186/s12967-016-0956-z27370270LiYGuoDLuGMohiuddin ChowdhuryATMZhangDRenMChenYWangRHeSLncRNA SNAI3-AS1 promotes PEG10-mediated proliferation and metastasis via decoying of miR-27a-3p and miR-34a-5p in hepatocellular carcinomaCell Death Dis11685202010.1038/s41419-020-02840-z32826862LiBShiCLiBZhaoJMWangLThe effects of Curcumin on HCT-116 cells proliferation and apoptosis via the miR-491/PEG10 pathwayJ Cell Biochem11930913098201810.1002/jcb.2644929058812YeMZhaoLZhangLWuSLiZQinYLinFPanLLncRNA NALT1 promotes colorectal cancer progression via targeting PEG10 by sponging microRNA-574-5pCell Death Dis13960202210.1038/s41419-022-05404-536385135Jiménez MartínOSchlosserAFurtwänglerRWegertJGesslerMMYCN and MAX alterations in Wilms tumor and identification of novel N-MYC interaction partners as biomarker candidatesCancer Cell Int21555202110.1186/s12935-021-02259-234689785LiCMMargolinAASalasMMemeoLMansukhaniMHibshooshHSzabolcsMKlinakisATyckoBPEG10 is a c-MYC target gene in cancer cellsCancer Res66665672200610.1158/0008-5472.CAN-05-155316423995WangCXiaoYHuZChenYLiuNHuGPEG10 directly regulated by E2Fs might have a role in the development of hepatocellular carcinomaFEBS Lett58227932798200810.1016/j.febslet.2008.07.00918625225PengYPZhuYYinLDZhangJJWeiJSLiuXLiuXCGaoWTJiangKRMiaoYPEG10 overexpression induced by E2F-1 promotes cell proliferation, migration, and invasion in pancreatic cancerJ Exp Clin Cancer Res3630201710.1186/s13046-017-0500-x28193232ZhangMSuiCDaiBShenWLuJYangJPEG10 is imperative for TGF-β1-induced epithelial-mesenchymal transition in hepatocellular carcinomaOncol Rep37510518201710.3892/or.2016.528228004118ZhangBLiuZYWuRZhangCMCaoKShanWGLiuZJiMTianZLSethiGTranscriptional regulator CTR9 promotes hepatocellular carcinoma progression and metastasis via increasing PEG10 transcriptional activityActa Pharmacol Sin4321092118202210.1038/s41401-021-00812-334876700YahiroYMaedaSShinoharaNJokojiGSakumaDSetoguchiTIshidouYNaganoSKomiyaSTaniguchiNPEG10 counteracts signaling pathways of TGF-β and BMP to regulate growth, motility and invasion of SW1353 chondrosarcoma cellsJ Bone Miner Metab37441454201910.1007/s00774-018-0946-830094509ShinoharaNMaedaSYahiroYSakumaDMatsuyamaKImamuraKKawamuraISetoguchiTIshidouYNaganoSKomiyaSTGF-β signalling and PEG10 are mutually exclusive and inhibitory in chondrosarcoma cellsSci Rep713494201710.1038/s41598-017-13994-w29044189RotinenMYouSYangJCoetzeeSGReis-SobreiroMHuangWCHuangFPanXYáñezAHazelettDJONECUT2 is a targetable master regulator of lethal prostate cancer that suppresses the androgen axisNat Med2418871898201810.1038/s41591-018-0241-130478421ChatterjeeAGallentBKatikiMQianCHarterMRSillettiSKomivesEAFreemanMRMuraliRThe homeodomain regulates stable DNA binding of prostate cancer target ONECUT2Nat Commun159037202410.1038/s41467-024-53159-839426953AkamatsuSInoueTOgawaOGleaveMEClinical and molecular features of treatment-related neuroendocrine prostate cancerInt J Urol25345351201810.1111/iju.1352629396873FengHChengASTsangDPLiMSGoMYCheungYSZhaoGJNgSSLinMCYuJCell cycle-related kinase is a direct androgen receptor-regulated gene that drives β-catenin/T cell factor-dependent hepatocarcinogenesisJ Clin Invest12131593175201110.1172/JCI4596721747169QinJLiuMDingQJiXHaoYWuXXiongJThe direct effect of estrogen on cell viability and apoptosis in human gastric cancer cellsMol Cell Biochem39599107201410.1007/s11010-014-2115-224934239KreutzDSinthuvanichCBileckAJankerLMuqakuBSlanyAGernerCCurcumin exerts its antitumor effects in a context dependent fashionJ Proteomics1826572201810.1016/j.jprot.2018.05.00729751106XuPWuZYangWWangLDysregulation of DNA methylation and expression of imprinted genes in mouse placentas of fetal growth restriction induced by maternal cadmium exposureToxicology390109116201710.1016/j.tox.2017.08.00328823913WuJJCaiAGreensladeJEHigginsNRFanCLeNTTTatmanMWhiteleyAMPradoMADieriksBVALS/FTD mutations in UBQLN2 impede autophagy by reducing autophagosome acidification through loss of functionProc Natl Acad Sci USA1171523015241202010.1073/pnas.191737111732513711ZhaoHGaoYMiaoJChenSLiJLiZYinCYueWSingle-cell RNA-seq highlights a specific carcinoembryonic cluster in ovarian cancerCell Death Dis121082202110.1038/s41419-021-04358-434775482LuxABeilCMajetyMBarronSGallioneCJKuhnHMBergJNKioschisPMarchukDAHafnerMHuman retroviral gag- and gag-pol-like proteins interact with the transforming growth factor-beta receptor activin receptor-like kinase 1J Biol Chem28084828493200510.1074/jbc.M40919720015611116LiuZTianZCaoKZhangBWenQZhouXYangWWangTShiHWangRTSG101 promotes the proliferation, migration and invasion of hepatocellular carcinoma cells by regulating the PEG10J Cell Mol Med237082201910.1111/jcmm.1387830450735XiongJQinJZhengYPengXLuoYMengXPEG10 promotes the migration of human Burkitt's lymphoma cells by up-regulating the expression of matrix metalloproteinase-2 and −9Clin Invest Med35E117125201210.25011/cim.v35i3.1658722673314GoldaMMótyánJAMahdiMTőzsérJFunctional study of the Retrotransposon-Derived human PEG10 ProteaseInt J Mol Sci212424202010.3390/ijms2107242432244497OkabeHSatohSFurukawaYKatoTHasegawaSNakajimaYYamaokaYNakamuraYInvolvement of PEG10 in human hepatocellular carcinogenesis through interaction with SIAH1Cancer Res6330433048200312810624TangYWuYXueMZhuBFanWLiJA 10-Gene signature identified by machine learning for predicting the response to transarterial chemoembolization in patients with hepatocellular carcinomaJ Oncol20223822773202210.1155/2022/382277335111225BangHHaSYHwangSHParkCKExpression of PEG10 is associated with poor survival and tumor recurrence in hepatocellular carcinomaCancer Res Treat47844852201510.4143/crt.2014.12425687862PengWZhaoGMaYYuHWangXDendritic cells transfected with PEG10 recombinant adenovirus elicit anti-tumor immune response in vitro and in vivoVaccine2935013506201110.1016/j.vaccine.2011.02.02721352943JieXLangCJianQChaoqunLDehuaYYiSYanpingJLuokunXQiupingZHuiWAndrogen activates PEG10 to promote carcinogenesis in hepatic cancer cellsOncogene2657415751200710.1038/sj.onc.121036217369855JiaHLYeQHQinLXBudhuAForguesMChenYLiuYKSunHCWangLLuHZGene expression profiling reveals potential biomarkers of human hepatocellular carcinomaClin Cancer Res1311331139200710.1158/1078-0432.CCR-06-102517317821IpWKLaiPBWongNLSySMBeheshtiBSquireJAWongNIdentification of PEG10 as a progression related biomarker for hepatocellular carcinomaCancer Lett250284291200710.1016/j.canlet.2006.10.01217126992WuXWangLFengFTianSWeighted gene expression profiles identify diagnostic and prognostic genes for lung adenocarcinoma and squamous cell carcinomaJ Int Med Res48300060519893837202010.1177/030006051989383731854219DengXHuYDingQHanRGuoQQinJLiJXiaoRTianSHuWPEG10 plays a crucial role in human lung cancer proliferation, progression, prognosis and metastasisOncol Rep3221592167201410.3892/or.2014.346925199998SinhaAZouYPatelASYooSJiangFSatoTKongRWatanabeHZhuJMassionPPEarly-stage lung adenocarcinoma MDM2 genomic amplification predicts clinical outcome and response to targeted therapyCancers (Basel)14708202210.3390/cancers1403070835158979WangDZhaoJLiSWeiJNanLMallampalliRKWeathingtonNMMaHZhaoYPhosphorylated E2F1 is stabilized by nuclear USP11 to drive Peg10 gene expression and activate lung epithelial cellsJ Mol Cell Biol106073201810.1093/jmcb/mjx03428992046NakagawaNMiyakeNOchiNYamaneHTakeyamaMNagasakiYIkedaTYokotaEFukazawaTNakanishiHTargeting ROR1 in combination with osimertinib in EGFR mutant lung cancer cellsExp Cell Res409112940202110.1016/j.yexcr.2021.11294034808132De MarcoCLaudannaCRinaldoNOliveiraDMRavoMWeiszACeccarelliMCairaERizzutoAZoppoliPSpecific gene expression signatures induced by the multiple oncogenic alterations that occur within the PTEN/PI3K/AKT pathway in lung cancerPLoS One12e0178865201710.1371/journal.pone.017886528662101XingQLiuSLuanJWangYMaLA novel 13 RNA binding proteins (RBPs) signature could predict prostate cancer biochemical recurrencePathol Res Pract225153587202110.1016/j.prp.2021.15358734419719Lundin-StrömKBBiloglavALazarevicVBehrendtzMCastorAJohanssonBParental origin of monosomy 7 in acute leukaemiaBr J Haematol192e132e135202110.1111/bjh.1735633548143YoshieHSedukhinaASMinagawaKOdaKOhnumaSYanagisawaNMaedaITakagiMKudoHNakazawaRA bioinformatics-to-clinic sequential approach to analysis of prostate cancer biomarkers using TCGA datasets and clinical samples: A new method for precision oncology?Oncotarget89960199611201710.18632/oncotarget.2044829245927ShapovalovaMLeeJKLiYVander GriendDJColemanIMNelsonPSDehmSMLeBeauAMPEG10 Promoter-driven expression of reporter genes enables molecular imaging of lethal prostate cancerCancer Res7956685680201910.1158/0008-5472.CAN-19-218131530569KimSThaperDBidnurSTorenPAkamatsuSBishopJLColinsCVahidSZoubeidiAPEG10 is associated with treatment-induced neuroendocrine prostate cancerJ Mol Endocrinol633949201910.1530/JME-18-022631013476HuCXiongJZhangLHuangBZhangQLiQYangMWuYWuQShenQPEG10 activation by co-stimulation of CXCR5 and CCR7 essentially contributes to resistance to apoptosis in CD19+CD34+ B cells from patients with B cell lineage acute and chronic lymphocytic leukemiaCell Mol Immunol1280294200416225771WuHLuoHWangMDuYLiJNAP1L5 promotes epithelial-mesenchymal transition by regulating PEG10 expression in acute myeloid leukaemiaLeuk Res148107623202510.1016/j.leukres.2024.10762339579659HaiderZLandforsMGolovlevaIErlansonMSchmiegelowKFlægstadTKanervaJNorén-NyströmUHultdinMDegermanSDNA methylation and copy number variation profiling of T-cell lymphoblastic leukemia and lymphomaBlood Cancer J1045202010.1038/s41408-020-0310-932345961XiongSLiuFSunJGaoSWongCCLTuPWangYAbrogation of USP9X is a potential strategy to decrease PEG10 levels and impede tumor progression in cutaneous T-cell lymphomaJ Invest Dermatol14427782788.e9202410.1016/j.jid.2024.02.03938677662KainzBShehataMBilbanMKienleDHeintelDKrömer-HolzingerELeTKröberAHellerGSchwarzingerIOverexpression of the paternally expressed gene 10 (PEG10) from the imprinted locus on chromosome 7q21 in high-risk B-cell chronic lymphocytic leukemiaInt J Cancer12119841993200710.1002/ijc.2292917621626AlanaziIHoffmannPAdelsonDLMicroRNAs are part of the regulatory network that controls EGF induced apoptosis, including elements of the JAK/STAT pathway, in A431 cellsPLoS One10e0120337201510.1371/journal.pone.012033725781916LeeYParkSLeeSHLeeHCharacterization of genetic aberrations in a single case of metastatic thymic adenocarcinomaBMC Cancer17330201710.1186/s12885-017-3282-928506304YanSDuLJiangXDuanWLiJXieYZhanYZhangSWangLLiSWangCEvaluation of serum exosomal lncRNAs as diagnostic and prognostic biomarkers for esophageal squamous cell carcinomaCancer Manag Res1297539763202010.2147/CMAR.S25097133116835GeHYanYWuDHuangYTianFPrognostic value of PEG10 in Asian solid tumors: A meta-analysisClin Chim Acta483197203201810.1016/j.cca.2018.04.04129727698SumitaniNIshidaKSawadaKKimuraTKanedaYNimuraKIdentification of malignant cell populations associated with poor prognosis in High-grade serous ovarian cancer using Single-Cell RNA sequencingCancers (Basel)143580202210.3390/cancers1415358035892844GovECo-expressed functional module-related genes in ovarian cancer stem cells represent novel prognostic biomarkers in ovarian cancerSyst Biol Reprod Med66255266202010.1080/19396368.2020.175973032441533HuaYMaXLiuXYuanXQinHZhangXIdentification of the potential biomarkers for the metastasis of rectal adenocarcinomaAPMIS12593100201710.1111/apm.1263328028826WatsonKMGardnerIHByrneRMRuhlRRLanciaultCPDeweyENAnandSTsikitisVLDifferential expression of PEG10 contributes to aggressive disease in early versus Late-onset colorectal cancerDis Colon Rectum6316101620202010.1097/DCR.000000000000177433149023KawaiYImadaKAkamatsuSZhangFSeilerRHayashiTLeongJBeraldiESaxenaNKretschmerAPaternally expressed gene 10 (PEG10) promotes growth, invasion, and survival of bladder cancerMol Cancer Ther1922102220202010.1158/1535-7163.MCT-19-103132847979LiuZYangZLiuDLiDZouQYuanYLiJLiangLChenMChenSTSG101 and PEG10 are prognostic markers in squamous cell/adenosquamous carcinomas and adenocarcinoma of the gallbladderOncol Lett711281138201410.3892/ol.2014.188624944680LiuDCYangZLJiangSIdentification of PEG10 and TSG101 as carcinogenesis, progression, and poor-prognosis related biomarkers for gallbladder adenocarcinomaPathol Oncol Res17859866201110.1007/s12253-011-9394-721455631LiXXiaoRTemboKHaoLXiongMPanSYangXYuanWXiongJZhangQPEG10 promotes human breast cancer cell proliferation, migration and invasionInt J Oncol4819331942201610.3892/ijo.2016.340626934961KatuwalNBKangMSGhoshMHongSDJeongYGParkSMKimSGSohnJKimTHMoonYWTargeting PEG10 as a novel therapeutic approach to overcome CDK4/6 inhibitor resistance in breast cancerJ Exp Clin Cancer Res42325202310.1186/s13046-023-02903-x38017459TangFHChangWATsaiEMTsaiMJKuoPLInvestigating novel genes potentially involved in endometrial adenocarcinoma using Next-generation sequencing and bioinformatic approachesInte J Med Sci1613381348201910.7150/ijms.3821931692912Sharan SinghSKumarRSingh KushwahaVBhattMLBBSinghAMishraARamHParmarDGuptaRExpression of radioresistant gene PEG10 in OSCC patients and its prognostic significanceAsian Pac J Cancer Prev1815131518201728669160LiangJLiuNXinHKnockdown long non-coding RNA PEG10 inhibits proliferation, migration and invasion of glioma cell line U251 by regulating miR-506Gen Physiol Biophys38295304201910.4149/gpb_201901831241046DengHXChenWHongSTBoycottKMGorrieGHSiddiqueNYangYFectoFShiYZhaiHMutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementiaNature477211215201110.1038/nature1035321857683KimSHNicholsKDAndersonENLiuYRameshNJiaWKuerbisCJScalfMSmithLMPandeyUBTibbettsRSAxon guidance genes modulate neurotoxicity of ALS-associated UBQLN2Elife12e84382202310.7554/eLife.8438237039476WhiteleyAMPradoMAde PootSAHPauloJAAshtonMDominguezSWeberMNguHSzpytJJedrychowskiMPGlobal proteomics of Ubqln2-based murine models of ALSJ Biol Chem296100153202110.1074/jbc.RA120.01596033277362HuberFArnaudMStevensonBJMichauxJBenedettiFThevenetJBobisseSChiffelleJGehertTMüllerMA comprehensive proteogenomic pipeline for neoantigen discovery to advance personalized cancer immunotherapyNat BiotechnolOctober112024(Epub ahead of print)10.1038/s41587-024-02420-y39394480TangQKhvorovaARNAi-based drug design: Considerations and future directionsNat Rev Drug Discov23341364202410.1038/s41573-024-00912-938570694HillCHBrierleyIStructural and functional insights into viral programmed ribosomal frameshiftingAnnu Rev Virol10217242202310.1146/annurev-virology-111821-12064637339768
Structure of PEG10. (A) Domain organization of PEG10. PEG10 mRNA produces two proteins, a PEG10-RF1 and a full-length PEG10-RF1/2. (B) Cartoon representation of PEG10-RF1/2 (AlphaFold: AF-I3NHH4-F1). Function of these domains: Coiled-coil domain (homomorphic and heteromorphic protein interaction), retrotransposon-gag domain (RNA binding), retroviruses zinc finger-like domain (DNA binding), retroviral aspartyl protease domain (self-cleavage) and reverse transcriptase domain (RNA binding). Brown ribbons represent the linker domain. RF, reading frame; PEG10, paternally expressed gene 10; pol, polymerase gene; gag, group-specific antigen gene.
Factors that regulate PEG10 expression. (A) Genetic regulation. (B) miRNAs bind to the 3′UTR of PEG10, which decreases mRNA stability. Circular RNA acts as a sponge for miRNA. (C) Transcriptional regulation of PEG10. (D) Degradation of PEG10 proteins. PEG10, paternally expressed gene 10; miRNA, microRNA; UBE3A, ubiquitin protein ligase E3A; UBQLN2, ubiquilin 2.