Open Access

Inhibiting proliferation and metastasis of osteosarcoma cells by downregulation of long non‑coding RNA colon cancer‑associated transcript 2 targeting microRNA‑143

Retraction in: /10.3892/ol.2023.13665

  • Authors:
    • Fengjiang Bi
    • Can Chen
    • Jing Fu
    • Lei Yu
    • Jia Geng
  • View Affiliations

  • Published online on: February 8, 2021     https://doi.org/10.3892/ol.2021.12526
  • Article Number: 265
  • Copyright: © Bi et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Osteosarcoma is a malignant bone tumor, which has a high incidence in children and adolescents. However, the pathogenesis of osteosarcoma remains unclear. Long noncoding RNA (lncRNA) is a new potential therapeutic target and diagnostic biomarker for osteosarcoma. Hence, the present study aimed to explore the effect of lncRNA colon cancer‑associated transcript (CCAT2) on osteosarcoma and its potential underlying mechanisms. For this purpose, the proliferation of osteosarcoma cells was measured using the CCK‑8 assay. The scratch‑wound and cell invasion assays were used to determine the migration and invasion of osteosarcoma cells, respectively. LncRNA CCAT2 and microRNA (miR)‑143 binding sites were identified by the dual‑luciferase reporter assay. RNA and protein expression levels were detected by reverse‑transcription quantitative PCR and western blotting, respectively. Downregulation of lncRNA CCAT2 inhibited the proliferation, migration, and invasion of osteosarcoma cells. The findings also revealed that miR‑143 bound directly to lncRNA CCAT2. The expression of miR‑143 was upregulated by the knockdown of lncRNA CCAT2. Downregulation of the FOS‑like antigen 2 was also observed after knockdown of lncRNA CCAT2. The function of lncRNA CCAT2 in osteosarcoma cells was attenuated by co‑transfection with anti‑miR‑143 oligodeoxyribonucleotide. In conclusion, downregulation of lncRNA CCAT2 inhibited the proliferation and metastasis of osteosarcoma cells by targeting miR‑143. lncRNA CCAT2 was identified as a potential target for osteosarcoma treatment.

Introduction

Osteosarcoma is a malignant bone tumor that accounts for 1–2% of all cancer cases 012-2016) (1). Although surgical and chemotherapy approaches for osteosarcoma have been greatly improved, the 5-year survival rate (2009–2015) was only 67% (birth to age 14) and ~ 69% (ages 15–19) (1). Hence, it is essential to determine novel and effective therapeutic targets and prognostic biomarkers for osteosarcoma.

Long non-coding RNAs (lncRNAs) are transcripts that are >200 nucleotides long (2). The regulatory RNA is abnormally expressed in various cancers, such as prostate cancer, liver cancer and lung cancer, making it an emerging diagnostic biomarker and therapeutic target (36). Numerous lncRNAs have been deregulated, and it has been proven that some are important regulators for osteosarcoma, including lncRNA cancer susceptibility candidate 2, maternally expressed gene 3 (MEG3) and colon cancer-associated transcript 2 (CCAT2) (79).

CCAT2 an oncogene, is highly expressed in cervical, colorectum, and lung cancer (911). The expression of CCAT2 is related to cancer progression and associated with poor overall survival in patients with cervical and colorectal cancer (10,11). CCAT2 is upregulated in non-small cell lung cancer tissues and cells, and promotes tumorigenesis by upregulating Pokemon expression (9). It has been revealed that the expression of lncRNA CCAT2 is higher in osteosarcoma tissues compared with that in adjacent normal tissues (12). High expression of lncRNA CCAT2 is related to larger tumor size, advanced stage, poor overall survival time and rate of patients with osteosarcoma (12). Similarly, Yan et al (13) also demonstrated that high expression of CCAT2 is associated with poor disease-free survival time and overall survival time in patients with osteosarcoma. In addition, lncRNA CCAT2 is upregulated in osteosarcoma cell lines (SOSP-9607, MG-63, U2OS, and SAOS-2) compared with a normal osteoblast cell line (hFOB) (13). Cell invasion is promoted by the overexpression of lncRNA CCAT2, and at least partially related to the upregulation of glycogen synthase kinase 3 β, large tumor suppressor 2 and c-Myc expression (12,13). However, the therapeutic potential and underlying mechanism regulating lncRNA CCAT2 in osteosarcoma remains elusive.

The present study was aimed to explore the therapeutic potential and molecular mechanism of CCAT2 in osteosarcoma. lncRNA CCAT2 may be a new potential target in the therapeutic of osteosarcoma.

Materials and methods

Cell culture

Human osteosarcoma cell lines (MG63 and U2OS) were obtained from The Cell Bank of Type Culture Collection of The Chinese Academy of Sciences and cultured in RPMI-1640 medium (Gibco; Thermo Fisher Scientific Inc.) with 10% FBS, 100 U/ml penicillin and 100 µg/ml streptomycin (Thermo Fisher Scientific Inc.). 293 T cells (Shanghai Gaining Biological Technology Co., Ltd.) were cultured in high-glucose DMEM medium with 10% FBS, which was used in luciferase reporter assay. All cells were cultured in an incubator under a water-saturated atmosphere of 5% CO2−95% air at 37°C.

Cell transfection

MG63 and U2OS cells (seeded in 12-well plates) were transfected with small interfering (si)-CCAT2 (Guangzhou RiboBio Co., Ltd.), anti-microRNA (miR)-143 oligodeoxyribonucleotide (AMO-143) (Ibsbio), or corresponding negative control (NC) sequences (scrambled sequences) 0.2 nmol/well at room temperature using the X-treme GENE siRNA transfection reagent according to the manufacturer's instructions (Roche Applied Science) and then cultured in an incubator in 5% CO2−95% air at 37°C. Subsequent experimentation was performed within 48 h after transfection. The sequences were as follows. si-CCAT2, 5′-ACUCAUUGGUUCCUUUAAGGG-3′ and 5′-CUUAAAGGAACCAAUGAGUCC-3′; si-NC, 5′-ACAUCAUAGUCGAACUUUATT-3′ and 5′-GAAAAGGACACUAUGCGGCTT-3′; AMO-143, 5′-GCUACAGUGCUUCAUCUCAUU-3′ and AMO-NC, 5′-UACUCUUUCUAGGAGGUUGUGAUU-3′. Subsequent experimentation was performed within 48 h after transfection.

CCK-8 assay

Proliferation of the MG63 and U2OS cells was evaluated using Cell Counting Kit-8 (CCK-8) (Dojindo Molecular Technologies Inc.). Cells were cultured for 2 h with the CCK-8 reagent prior to detection. The detailed procedure was described previously (12).

Wound healing assay

MG63 and U2OS cCells were inoculated into a 12-well culture plate (4×105/well) in a monolayer. The cells were cultured with RPMI-1640 medium with 10% FBS (14,15). A straight line was then scratched on the monolayer surface (confluence of 70–80%) using a pipette tip (16). After treatment, the wells were washed twice to remove the dead cells from the medium. The width of the wound, which reflects the migration of the cells, was measured using a light microscope (Leica Microsystems GmbH) within 48 h.

Boyden chamber cell invasion assay

MG63 and U2OS cells (1.5×104/well) were inoculated into the upper chamber (RPMI-1640 medium without serum) of a 24-well Transwell plate (BD Biosiences), which was coated with BD Matrigel (BD Biosiences) for 5 h at 37°C. RPMI-1640 medium with 10% FBS was added to the lower chambers. Subsequently, 48 h after incubation at 37°C, invading cells in the lower chamber were stained with 0.1% crystal violet solution for 15 min at room temperature and the images was captured using a light microscope (Leica Microsystems GmbH).

Reverse transcription-quantitative (RT-q) PCR

Total RNA was extracted from MG63 and U2OS cells using TRIzol® reagent (Roche Applied Science). cDNA was synthesized using the Takara reverse transcriptase kit (Takara Bio Inc.) according to the manufacturer's instructions. The reverse transcription steps were as follows: 3 cycles of 30°C for 10 min followed by 3 cycles of 50°C for 60 min followed by 95°C for 5 min and 4°C holding. The cDNA strand was amplified by RT-qPCR using SYBR-Green I (Toyobo Life Science) on a 7500 fast RT-qPCR system (Applied Biosystems; Thermo Fisher Scientific, Inc.). The thermocycling conditions were as follows: 60 sec at 95°C followed by 40 cycles of 15 sec at 95°C, 15 sec at 60°C and 45 sec at 72°C. GAPDH and U6 were used as internal references for mRNA or miRNA, respectively. The primer sequences were as follows. CCAT2, forward 5′-CCCTGGTCAAATTGCTTAAC-3′ and reverse, 5′-TTATTCGTCCCTCTGTTTTATGG-3′; GAPDH, forward 5′-CCACATCGCTCAGACACC-3′ and reverse, 5′-ACCAGGCGCCCAATA-3′; miR-143, forward 5′-AGCGTGTGTCGTGGAGTC-3′ and reverse, 5′-TCGTGAGATGAAGCACTGTAG-3′; U6, forward 5′-CTCGCTTCGGCAGCACA-3′ and reverse, 5′-AACGCTTCACGAATTTGCGT-3′; and FOS-Like antigen 2 (FOSL2), forward 5′-GAGAGGAACAAGCTGGCTGC-3′ and reverse, 5′-GCTTCTCCTTCTCCTTCTGC-3′. The results were analyzed by the 2−ΔΔCq method (17).

Western blotting

Total protein was exacted from MG63 and U2OS cells using RIPA Buffer (Beyotime Institute of Biotechnology) and quantified using a BCA kit (Beyotime Institute of Biotechnology). The proteins (20 µg per lane) were separated by 10% SDS-PAGE and transferred onto a nitrocellulose membrane. The nitrocellulose membrane was blocked with 5% skimmed milk for 2 h at room temperature. The membrane was incubated at 4°C with primary antibodies against FOSL2 (1:1,000; cat. no. PB0624; Wuhan Boster Biological Technology, Ltd.) and GAPDH (1:2,000; cat. no. TA890003; Origene Technologies Inc.) overnight, and incubated with anti-Rabbit IgG with ECM solution (1:5,000; cat. no. EK1002; Wuhan Boster Biological Technology, Ltd.) for 1 h at room temperature. The bands were visualized using ECM solution (Wuhan Boster Biological Technology, Ltd.). GAPDH was used as the internal loading control. The protein bands on the membrane were developed and quantified using Quantity One software v.4.6.2 (Bio-Rad Laboratories Inc.) (18).

Luciferase reporter assay

lncRNA CCAT2 (gene name: CCAT2, Ensembl ID: ENSG00000280997) target was predicted using LncBase Predicted v.2 (http://carolina.imis.athena-innovation.gr/diana_tools/web/index.php?r=lncbasev2/index-predicted). The results indicated that miR-143 could bind to lncRNA CCAT2. 293T cells (2×104/well) plated in a 24-well plate, were co-transfected with plasmids with wilt type CCAT2 (CCAT2-wt) or mutated CCAT2 (CCAT2-mut) (psiCHECKTM-2 Vector; Promega Corporation) (psiCHECK™-2 Vector; Promega Corporation) and miR-143 mimic or miR-NC (Ibsbio) by Lipofectamine® 2000 (Thermo Fisher Scientific, Inc.). The sequences were as follows: miR-143, 5′-UGAGAUGAAGCACUGUAGCUC-3′ and miR-NC 5′-UCACAACCUCCUAGAAAGAGUAGA-3′. Luciferase activity was detected 24 h after transfection by the Dual-Luciferase Reporter Assay System (Promega Corporation). Renilla luciferase activity was normalized with CCAT2-wt + miR-NC group.

Statistical analysis

Data are presented as the mean ± standard deviation of at least 3 biological replicates. All data were analyzed using GraphPad Prism v.8 (GraphPad Software Inc.). The comparison of results among groups was performed by analysis of variance (ANOVA) and followed by the post hoc Tukey's multiple comparisons test. P<0.05 was considered to indicate a statistically significant difference.

Results

Downregulation of lncRNA CCAT2 inhibits the proliferation of osteosarcoma cells

LncRNA CCAT2 expression has been demonstrated to be higher in osteosarcoma tissues and cell lines compared with that in adjacent normal tissues and osteoblastic cell line, respectively (12,13). Compared with siNC group, lncRNA CCAT2 expression was downregulated after transfected with siRNA against CCAT2 in MG63 and U2OS cells (Fig. 1A and B). The proliferation of MG63 and U2OS cells was significantly inhibited by the downregulation of lncRNA CCAT2 compared with the siNC group (Fig. 1C and D).

Downregulation of lncRNA CCAT2 hampers the migration capability and invasion of osteosarcoma cells

Knockdown of lncRNA CCAT2 significantly inhibited the migration of MG63 and U2OS cells in the wound healing (Fig. 2A-D) and Boyden chamber cell invasion assays (Fig. 2E-H). The MG63 cell line had a more profoundly inhibited migration capability compared with U2OS cells (Fig. 2A-D).

Downregulation of CCAT2 upregulates miR-143 expression in osteosarcoma cells

LncBase Predicted v.2 software predicted that there were 3 binding sites between miR-143 and lncRNA CCAT2 (Fig. 3A). After transfection with miR-143 mimics, luciferase activity of 293T cells containing CCAT2-wild-type (CCAT2-wt) was lower compared with 293T cells containing the CCAT2-mutant (CCAT2-mut), which indicated that miR-143 could directly bind to lncRNA CCAT2 (Fig. 3B). In concert, miR-143 expression in MG63 and U2OS cells was significantly upregulated by downregulation of lncRNA CCAT2 (Fig. 3C and D).

Knockdown of miR-143 attenuates the effects of downregulation of lncRNA CCAT2 in osteosarcoma cells

Effects of lncRNA CCAT2 downregulation (si-CCAT2+AMO-NC group) on proliferation were attenuated by co-transfection with AMO-143 (si-CCAT2+AMO-143 group) in osteosarcoma cells (Fig. 4A and B). Similarly, the effects of lncRNA CCAT2 downregulation (si-CCAT2+AMO-NC group) on migration and invasion were attenuated by co-transfection with AMO-143 (si-CCAT2+AMO-143 group) in osteosarcoma cells (Fig. 4C-F).

Downregulation of lncRNA CCAT2 inhibits FOSL2 expression by regulating miR-143 expression in osteosarcoma cells

FOSL2 is a target of miR-143 (19). The transfection of AMO-143 downregulated miR-143 expression compared with negative controls (Fig. 5A). Simultaneously, the expression of FOSL2 was upregulated after the interference of miR-143 compared with negative controls (Fig. 5B). Taken together, the FOSL2 mRNA and protein expressions were decreased by knockdown of lncRNA CCAT2 (Fig. 5C and D). However, co-transfection with AMO-143 reversed the role of lncRNA CCAT2 knockdown in regulating FOSL2 expression in the MG63 and U2OS cells (Fig. 5E and F).

Discussion

Osteosarcoma is a malignant solid tumor with high incidence in children and adolescents (20,21). In the present study, the role and molecular mechanism of lncRNA CCAT2 in osteosarcoma cells was investigated and the results indicated that downregulation of lncRNA CCAT2 expression regulated miR-143 expression and inhibited the proliferation and metastasis of osteosarcoma cells.

Several studies have demonstrated that lncRNAs are major regulators of gene expression and essential in a variety of pathological procedures, including cancer, cardiovascular diseases and neuronal disorders (2225). In addition, the expression profiles of lncRNAs are altered in cancer (26,27). The role and therapeutic potential of cancer-related lncRNAs have become a research hotspot in recent years. Although a limited number of lncRNAs have been studied, researchers have made significant progress in studying the specific mechanism of lncRNA regulation. Recent studies have reported the role of lncRNAs in the generation and progression of cancers and how they can be used as biomarkers for diagnosis and treatment of cancers (2830).

CCAT2 is a new oncogenic lncRNA gene, which was first discovered in related studies on colon cancer (31). It was overexpressed in microsatellite-stable colorectal cancer to promote proliferation, metastasis, and chromosomal instability of the tumor (31). The effect of lncRNA CCAT2 has been demonstrated in different types of cancers. For example, lncRNA CCAT2 has been reported to be upregulated in lung cancer, which not only promotes the generation and progression of lung cancer, but is also considered to be a predictive factor for prognosis (9,32). LncRNA CCAT2 expression is related to poor prognosis in patients with gastric cancer (33,34). The expression of lncRNA CCAT2 is higher in hepatocellular carcinoma cell lines compared with that in normal liver epithelial cells (35). In addition, the high expression of CCAT2 significantly suppressed hepatocellular carcinoma cell apoptosis (3537).

LncRNA CCAT2 expression is significantly higher in osteosarcoma tissues and cells compared with that in normal tissues and cells (12,13). In the present study, to investigate the role of lncRNA CCAT2 in osteosarcoma cells, the expression of lncRNA CCAT2 was downregulated using siRNA. This resulted in the inhibition of proliferation and migration of osteosarcoma cells in the present study. LncRNA CCAT2, a competitive endogenous RNA can regulate gene expression by sponging miRNAs (38). In the present study, an online software, LncBase Predicted v.2, predicted that lncRNA CCAT2 has three miR-143 binding sites. Subsequently, a direct interaction between lncRNA CCAT2 and miR-143 was revealed in the dual-luciferase reporter assay. In concert, in the present study miR-143 expression was significantly upregulated by the downregulation of lncRNA CCAT2.

miR-143 is a tumor-suppressor miRNA in colon cancer, breast cancer and pancreatic cancer, etc (3941). In addition, the proliferation and migration of osteosarcoma cells have been demonstrated to be inhibited by the upregulation of miR-143 (42,43). In the present study, to confirm the effect of miR-143 regulation on lncRNA CCAT2, miR-143 expression was downregulated using AMO-143. The findings of the present study revealed that downregulation of lncRNA CCAT2 inhibited tumor proliferation and metastasis by regulating miR-143.

Recent studies have suggested that miR-143 expression is decreased in osteosarcoma tissues and cell lines (MG-63 and 143B) compared with that in adjacent normal tissues and osteoblastic cell line (hFOB 1.19), respectively (19,44). In addition, FOSL2, also known as Fra-2 is associated with metastasis in breast and lung cancer (42,43). Tumor proliferation and migration was inhibited by upregulation of miR-143 targeting FOSL2 (19). In accordance with this, the present study also demonstrated that the inhibition of miR-143 could upregulate FOSL2 mRNA expression in osteosarcoma cells.

Subsequently, in the present study the effect of regulation of lncRNA CCAT2 on FOSL2 expression was studied and it was revealed that FOSL2 expression was inhibited by the downregulation of lncRNA CCAT2, whereas co-transfection with AMO-143 reversed the effect of lncRNA CCAT2 on FOSL2. Hence, the downregulation of lncRNA CCAT2 inhibited FOSL2 expression through the upregulation of miR-143.

In conclusion, the present study improved understanding of the pathogenesis of osteosarcoma. In addition, the findings of the present study indicated that lncRNA CCAT2 may be a new potential therapeutic target for osteosarcoma. An improved understanding of the importance of deregulated lncRNAs will definitely improve osteosarcoma prevention and treatment.

Acknowledgements

Not applicable.

Funding

No funding was received.

Availability of data and materials

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

Authors' contributions

FB and JG conceived the study and designed the experiments. CC, JF and LY contributed to the data collection; performed the data analysis and interpreted the results. FB wrote the manuscript. JG revised the manuscript for important intellectual content. All authors read and approved the final manuscript.

Ethics approval and consent to participate

Not applicable.

Consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interests.

References

1 

Siegel RL, Miller KD and Jemal A: Cancer statistics, 2020. CA Cancer J Clin. 70:7–30. 2020. View Article : Google Scholar : PubMed/NCBI

2 

Ratti M, Lampis A, Ghidini M, Salati M, Mirchev MB, Valeri N and Hahne JC: MicroRNAs (miRNAs) and long non-coding RNAs (lncRNAs) as new tools for cancer therapy: first steps from bench to bedside. Target Oncol. 15:261–278. 2020. View Article : Google Scholar : PubMed/NCBI

3 

Gutschner T, Richtig G, Haemmerle M and Pichler M: From biomarkers to therapeutic targets-the promises and perils of long non-coding RNAs in cancer. Cancer Metastasis Rev. 37:83–105. 2018. View Article : Google Scholar : PubMed/NCBI

4 

Shi X, Zhang W, Nian X, Lu X, Li Y, Liu F, Wang F, He B, Zhao L, Zhu Y, et al: The previously uncharacterized lncRNA APP promotes prostate cancer progression by acting as a competing endogenous RNA. Int J Cancer. 146:475–486. 2020. View Article : Google Scholar : PubMed/NCBI

5 

Wang H, Huo X, Yang XR, He J, Cheng L, Wang N, Deng X, Jin H, Wang N, Wang C, et al: STAT3-mediated upregulation of lncRNA HOXD-AS1 as a ceRNA facilitates liver cancer metastasis by regulating SOX4. Mol Cancer. 16:1362017. View Article : Google Scholar : PubMed/NCBI

6 

Pan J, Fang S, Tian H, Zhou C, Zhao X, Tian H, He J, Shen W, Meng X, Jin X, et al: lncRNA JPX/miR-33a-5p/Twist1 axis regulates tumorigenesis and metastasis of lung cancer by activating Wnt/β-catenin signaling. Mol Cancer. 19:92020. View Article : Google Scholar : PubMed/NCBI

7 

Ba Z, Gu L, Hao S, Wang X, Cheng Z and Nie G: Downregulation of lncRNA CASC2 facilitates osteosarcoma growth and invasion through miR-181a. Cell Prolif. 51:e124092018. View Article : Google Scholar

8 

Shen B, Zhou N, Hu T, Zhao W, Wu D and Wang S: LncRNA MEG3 negatively modified osteosarcoma development through regulation of miR-361-5p and FoxM1. J Cell Physiol. 234:13464–13480. 2019. View Article : Google Scholar : PubMed/NCBI

9 

Zhao Z, Wang J, Wang S, Chang H, Zhang T and Qu J: LncRNA CCAT2 promotes tumorigenesis by over-expressed Pokemon in non-small cell lung cancer. Biomed Pharmacother. 87:692–697. 2017. View Article : Google Scholar : PubMed/NCBI

10 

Chen X, Liu L and Zhu W: Up-regulation of long non-coding RNA CCAT2 correlates with tumor metastasis and poor prognosis in cervical squamous cell cancer patients. Int J Clin Exp Pathol. 8:13261–13266. 2015.PubMed/NCBI

11 

Zhang J, Jiang Y, Zhu J, Wu T, Ma J, Du C, Chen S, Li T, Han J and Wang X: Overexpression of long non-coding RNA colon cancer-associated transcript 2 is associated with advanced tumor progression and poor prognosis in patients with colorectal cancer. Oncol Lett. 14:6907–6914. 2017.PubMed/NCBI

12 

Ruan R and Zhao XL: LncRNA CCAT2 enhances cell proliferation via GSK3β/β-catenin signaling pathway in human osteosarcoma. Eur Rev Med Pharmacol Sci. 22:2978–2984. 2018.PubMed/NCBI

13 

Yan L, Wu X, Yin X, Du F, Liu Y and Ding X: LncRNA CCAT2 promoted osteosarcoma cell proliferation and invasion. J Cell Mol Med. 22:2592–2599. 2018. View Article : Google Scholar : PubMed/NCBI

14 

Zhang C, Ma K and Li WY: Cinobufagin suppresses the characteristics of osteosarcoma cancer cells by inhibiting the IL-6-OPN-STAT3 pathway. Drug Des Devel Ther. 13:4075–4090. 2019. View Article : Google Scholar : PubMed/NCBI

15 

Qu H, Xue Y, Lian W, Wang C, He J, Fu Q, Zhong L, Lin N, Lai L, Ye Z, et al: Melatonin inhibits osteosarcoma stem cells by suppressing SOX9-mediated signaling. Life Sci. 207:253–264. 2018. View Article : Google Scholar : PubMed/NCBI

16 

Eggers B, Marciniak J, Memmert S, Kramer FJ, Deschner J and Nokhbehsaim M: The beneficial effect of cold atmospheric plasma on parameters of molecules and cell function involved in wound healing in human osteoblast-like cells in vitro. Odontology. 108:607–616. 2020. View Article : Google Scholar : PubMed/NCBI

17 

Livak KJ and Schmittgen TD: Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods. 25:402–408. 2001. View Article : Google Scholar : PubMed/NCBI

18 

Chu Q, Jiang Y, Zhang W, Xu C, Du W, Tuguzbaeva G, Qin Y, Li A, Zhang L, Sun G, et al: Pyroptosis is involved in the pathogenesis of human hepatocellular carcinoma. Oncotarget. 7:84658–84665. 2016. View Article : Google Scholar : PubMed/NCBI

19 

Sun X, Dai G, Yu L, Hu Q, Chen J and Guo W: miR-143-3p inhibits the proliferation, migration and invasion in osteosarcoma by targeting FOSL2. Sci Rep. 8:6062018. View Article : Google Scholar : PubMed/NCBI

20 

Endicott AA, Morimoto LM, Kline CN, Wiemels JL, Metayer C and Walsh KM: Perinatal factors associated with clinical presentation of osteosarcoma in children and adolescents. Pediatr Blood Cancer. 64:642017. View Article : Google Scholar : PubMed/NCBI

21 

Strauss SJ and Whelan JS: Current questions in bone sarcomas. Curr Opin Oncol. 30:252–259. 2018. View Article : Google Scholar : PubMed/NCBI

22 

Rasmussen TP: Parallels between artificial reprogramming and the biogenesis of cancer stem cells: Involvement of lncRNAs. Semin Cancer Biol. 57:36–44. 2019. View Article : Google Scholar : PubMed/NCBI

23 

Rynkeviciene R, Simiene J, Strainiene E, Stankevicius V, Usinskiene J, Miseikyte Kaubriene E, Meskinyte I, Cicenas J and Suziedelis K: Non-coding RNAs in glioma. Cancers (Basel). 11:172018. View Article : Google Scholar

24 

Jiang Y, Du W, Chu Q, Qin Y, Tuguzbaeva G, Wang H, Li A, Li G, Li Y, Chai L, et al: Downregulation of long non-coding RNA Kcnq1ot1: an important mechanism of arsenic trioxide-induced long QT syndrome. Cell Physiol Biochem. 45:192–202. 2018. View Article : Google Scholar : PubMed/NCBI

25 

Ma N, Tie C, Yu B, Zhang W and Wan J: Identifying lncRNA-miRNA-mRNA networks to investigate Alzheimer's disease pathogenesis and therapy strategy. Aging (Albany NY). 12:2897–2920. 2020. View Article : Google Scholar : PubMed/NCBI

26 

Huang X, Ta N, Zhang Y, Gao Y, Hu R, Deng L, Zhang B, Jiang H and Zheng J: Microarray analysis of the expression profile of long non-coding RNAs indicates lncRNA RP11-263F15.1 as a biomarker for diagnosis and prognostic prediction of pancreatic ductal adenocarcinoma. J Cancer. 8:2740–2755. 2017. View Article : Google Scholar : PubMed/NCBI

27 

Wang H, Wu J, Zhang X, Ding L and Zeng Q: Microarray analysis of the expression profile of lncRNAs reveals the key role of lncRNA BC088327 as an agonist to heregulin 1β induced cell proliferation in peripheral nerve injury. Int J Mol Med. 41:3477–3484. 2018.PubMed/NCBI

28 

Li J, Zhu Y, Wang H and Ji X: Targeting long noncoding rna in glioma: a pathway perspective. Mol Ther Nucleic Acids. 13:431–441. 2018. View Article : Google Scholar : PubMed/NCBI

29 

Chen W, Hang Y, Xu W, Wu J, Chen L, Chen J, Mao Y, Song J, Song J and Wang H: BLACAT1 predicts poor prognosis and serves as oncogenic lncRNA in small-cell lung cancer. J Cell Biochem. 2018.

30 

Dai W, Mu L, Cui Y, Li Y, Chen P, Xie H and Wang X: Berberine promotes apoptosis of colorectal cancer via regulation of the long non-coding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2)/AU-binding factor 1 (AUF1)/B-cell CLL/lymphoma 2 (Bcl-2) axis. Med Sci Monit. 25:730–738. 2019. View Article : Google Scholar : PubMed/NCBI

31 

Ling H, Spizzo R, Atlasi Y, Nicoloso M, Shimizu M, Redis RS, Nishida N, Gafà R, Song J, Guo Z, et al: CCAT2, a novel noncoding RNA mapping to 8q24, underlies metastatic progression and chromosomal instability in colon cancer. Genome Res. 23:1446–1461. 2013. View Article : Google Scholar : PubMed/NCBI

32 

Chen S, Wu H, Lv N, Wang H, Wang Y, Tang Q, Shao H and Sun C: LncRNA CCAT2 predicts poor prognosis and regulates growth and metastasis in small cell lung cancer. Biomed Pharmacother. 82:583–588. 2016. View Article : Google Scholar : PubMed/NCBI

33 

Wu SW, Hao YP, Qiu JH, Zhang DB, Yu CG and Li WH: High expression of long non-coding RNA CCAT2 indicates poor prognosis of gastric cancer and promotes cell proliferation and invasion. Minerva Med. 108:317–323. 2017.PubMed/NCBI

34 

Wang CY, Hua L, Yao KH, Chen JT, Zhang JJ and Hu JH: Long non-coding RNA CCAT2 is up-regulated in gastric cancer and associated with poor prognosis. Int J Clin Exp Pathol. 8:779–785. 2015.PubMed/NCBI

35 

Zhou N, Si Z, Li T, Chen G, Zhang Z and Qi H: Long non-coding RNA CCAT2 functions as an oncogene in hepatocellular carcinoma, regulating cellular proliferation, migration and apoptosis. Oncol Lett. 12:132–138. 2016. View Article : Google Scholar : PubMed/NCBI

36 

Xu Y, Wang B, Zhang F, Wang A, Du X, Hu P, Zhu Y and Fang Z: Long non-coding RNA CCAT2 is associated with poor prognosis in hepatocellular carcinoma and promotes tumor metastasis by regulating Snail2-mediated epithelial-mesenchymal transition. OncoTargets Ther. 10:1191–1198. 2017. View Article : Google Scholar

37 

Chen F, Bai G, Li Y, Feng Y and Wang L: A positive feedback loop of long noncoding RNA CCAT2 and FOXM1 promotes hepatocellular carcinoma growth. Am J Cancer Res. 7:1423–1434. 2017.PubMed/NCBI

38 

Yu Y, Nangia-Makker P, Farhana L and Majumdar APN: A novel mechanism of lncRNA and miRNA interaction: CCAT2 regulates miR-145 expression by suppressing its maturation process in colon cancer cells. Mol Cancer. 16:1552017. View Article : Google Scholar : PubMed/NCBI

39 

Zhu H, Dougherty U, Robinson V, Mustafi R, Pekow J, Kupfer S, Li YC, Hart J, Goss K, Fichera A, et al: EGFR signals downregulate tumor suppressors miR-143 and miR-145 in Western diet-promoted murine colon cancer: Role of G1 regulators. Mol Cancer Res. 9:960–975. 2011. View Article : Google Scholar : PubMed/NCBI

40 

Yan X, Chen X, Liang H, Deng T, Chen W, Zhang S, Liu M, Gao X, Liu Y, Zhao C, et al: miR-143 and miR-145 synergistically regulate ERBB3 to suppress cell proliferation and invasion in breast cancer. Mol Cancer. 13:2202014. View Article : Google Scholar : PubMed/NCBI

41 

Hu Y, Ou Y, Wu K, Chen Y and Sun W: miR-143 inhibits the metastasis of pancreatic cancer and an associated signaling pathway. Tumour Biol. 33:1863–1870. 2012. View Article : Google Scholar : PubMed/NCBI

42 

Dong X, Lv B, Li Y, Cheng Q, Su C and Yin G: miR-143 regulates the proliferation and migration of osteosarcoma cells through targeting MAPK7. Arch Biochem Biophys. 630:47–53. 2017. View Article : Google Scholar : PubMed/NCBI

43 

Wang Q, Cai J, Wang J, Xiong C and Zhao J: miR-143 inhibits EGFR-signaling-dependent osteosarcoma invasion. Tumour Biol. 35:12743–12748. 2014. View Article : Google Scholar : PubMed/NCBI

44 

Liu H, Wang H, Liu H and Chen Y: Effect of miR-143 on the apoptosis of osteosarcoma cells. Int J Clin Exp Pathol. 8:14241–14246. 2015.PubMed/NCBI

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Bi F, Chen C, Fu J, Yu L and Geng J: Inhibiting proliferation and metastasis of osteosarcoma cells by downregulation of long non‑coding RNA colon cancer‑associated transcript 2 targeting microRNA‑143 Retraction in /10.3892/ol.2023.13665. Oncol Lett 21: 265, 2021.
APA
Bi, F., Chen, C., Fu, J., Yu, L., & Geng, J. (2021). Inhibiting proliferation and metastasis of osteosarcoma cells by downregulation of long non‑coding RNA colon cancer‑associated transcript 2 targeting microRNA‑143 Retraction in /10.3892/ol.2023.13665. Oncology Letters, 21, 265. https://doi.org/10.3892/ol.2021.12526
MLA
Bi, F., Chen, C., Fu, J., Yu, L., Geng, J."Inhibiting proliferation and metastasis of osteosarcoma cells by downregulation of long non‑coding RNA colon cancer‑associated transcript 2 targeting microRNA‑143 Retraction in /10.3892/ol.2023.13665". Oncology Letters 21.4 (2021): 265.
Chicago
Bi, F., Chen, C., Fu, J., Yu, L., Geng, J."Inhibiting proliferation and metastasis of osteosarcoma cells by downregulation of long non‑coding RNA colon cancer‑associated transcript 2 targeting microRNA‑143 Retraction in /10.3892/ol.2023.13665". Oncology Letters 21, no. 4 (2021): 265. https://doi.org/10.3892/ol.2021.12526