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Introduction

Non-SMC condensin I complex subunit G (NCAPG) was originally identified from nuclear extracts of HeLa cells (1). NCAPG has been shown to be involved in chromosomal organization and rearrangement via interaction with non-SMC condensin I complex subunit H (NCAPH) (2) and non-SMC condensin I complex subunit D2 (NCAPD2) (3) to form condensin complex I, which maintains the overall stability of chromosomes through participating in chromosome organization and rearrangement, and by promoting the correct segregation and accurate distribution of chromosomes during mitosis (4,5). Hara et al (2) found that the NCAPG-NCAPH subcomplex consists of the N-terminal domain of polypeptide human chromosome-associated polypeptide-G (hCAP-G) linked to its C-terminal domain and a fragment of polypeptide human chromosome-associated polypeptide-H (hCAP-H) containing motif IV. This subcomplex has the ability to interact with both double- and single-stranded DNA, contributing to the correct assembly and segregation of chromosomes. The homologue of the NCAPG subunit in Drosophila is the dCAP-G protein. The dCAP-G mutation results in delayed chromosome condensation at prometaphase, and failure of sister chromatid segregation at anaphase (6). Murphy and Sarge (7) found that the three potential phosphorylation sites on the hCAP-G subunit were Thr-308, Thr-332 and Thr-931, and mutation of these residues to alanine was demonstrated to affect the localization of NCAPG during mitosis.

However, it has been revealed that abnormal expression of NCAPG often affects the occurrence and development of a wide variety of tumours, including lung cancer (8,9), hepatocellular carcinoma (HCC) (10,11), colorectal cancer (12), pancreatic cancer (13,14), breast cancer (BC) (15), ovarian cancer (16), endometrial carcinoma (17), glioma (18), rhabdomyosarcoma (19) and melanoma (20). When NCAPG is highly expressed, the proliferation and invasion of tumours is promoted, and the expression level of NCAPG is negatively correlated with the prognosis of patients, suggesting that NCAPG is a factor that adversely affects the survival of patients with tumour. Surprisingly, NCAPG is expressed at low levels in basal cell carcinoma (BCC) (21), lymphoblastic acute myeloid leukemia (4) and multiple myeloma (22), and this may be associated with immune infiltration and reduced mitogenic gene expression, leading to cell proliferation arrest.

In HCC (11), colorectal cancer (12) and lung adenocarcinoma (LUAD) (23), NCAPG expression has been identified to be closely associated with the degree of lymph node metastasis, tumour clinical stage and tumour progression, and overexpression of NCAPG was associated with poor prognosis in these patients. In addition, high expression of NCAPG was associated with tumour infiltration of several immune cell types, including B cells and CD4 memory T cells in non-small cell lung cancer (NSCLC) (9) and neutrophils in HCC (24), suggesting accordingly that NCAPG fulfils an important role in regulating tumour immunity.

NCAPG has been reported to have pro-carcinogenic biological functions, including promoting tumour cell proliferation, cell cycle function, cell migration, in vivo tumour formation in mice and in vivo metastasis, and it has been proposed that this may be associated with cellular pathways, cell cycle, mismatch repair and cellular damage (25–28). Therefore, further study of the function and underlying mechanisms of NCAPG should enable improved understanding of the processes of tumourigenesis and development, in order to potentially provide novel targets and strategies for tumour therapy.

Role of NCAPG in tumourigenesis and development

Association between NCAPG and cell proliferation, apoptosis, migration and invasion

A large number of studies have demonstrated that NCAPG is able to regulate cell proliferation, apoptosis, migration and invasion. NCAPG has been shown to be overexpressed in HCC, and its level of expression correlates with clinicopathological features, such as recurrence, time to recurrence, metastasis, differentiation and tumour-node-metastasis staging (11). The long non-coding RNA (lncRNA) taurine-upregulated gene 1 (TUG1) was revealed to be overexpressed in HCC, where it mediates HCC cell growth, epithelial-mesenchymal transition (EMT) and metastasis (29). Li et al (30) found that TUG1 could target and regulate NCAPG, and the expression of NCAPG is negatively correlated with survival in HCC. It has been demonstrated that, upon knockdown of NCAPG, the expression levels of the cell cycle proteins A1 and CDK2, Bcl-2 and N-calmodulin are inhibited, causing the cell cycle to stall in the S-phase (11), resulting in a weakening of the ability of cells to migrate and invade (31), thereby inducing apoptosis. It has also been revealed that knockdown of NCAPG reduces cell viability, causes abnormal mitosis and mitochondrial fragmentation and promotes apoptosis (32). Ai et al (33) detected that the microRNA (miRNA) miR-181c was significantly downregulated in HCC and that the expression level of miR-181c was negatively correlated with the expression level of NCAPG. Knockdown of NCAPG was also found to result in decreased rates of cell proliferation, invasion and migration, a reduced level of EMT and the promotion of apoptosis.

A previously published study by Li et al (34) revealed that NCAPG is a key gene in castration-resistant prostate cancer (CRPC). In a previous study, Goto et al (35) showed that miR-145-3p was lowly expressed in CRPC tissues, where it acted as a negative regulator of NCAPG, thereby functioning as a tumour suppressor. Furthermore, the miRNA miR-99a-3p was found to significantly downregulate NCAPG expression in CRPC, suggesting that it may fulfil an important oncogenic function in CRPC (36).

Yu et al (37) reported that knockdown of NCAPG resulted in cell cycle blockade in the S and G2 phases of the cycle, which resulted in a marked decrease in the proliferative and invasive capabilities of ovarian cancer cells and in the induction of apoptosis.

Song et al (38) demonstrated that NCAPG is highly expressed in gastric cancer and is enriched in the cell cycle. NCAPG serves as a downstream target of miR-193b-3p, and it is negatively regulated by this miRNA; moreover, its overexpression was found to promote the proliferation of gastric cancer cells. Sun et al (39) found that the expression level of NCAPG in the tumour cells of patients with advanced gastric cancer was markedly increased compared with that in the early stage of the disease. Knockdown of NCAPG induced cell cycle arrest in G0/G1 phase, thereby inhibiting both the rates of cell proliferation, migration and invasion and EMT. Zhang et al (27) found that, in gastric cancer, silencing of NCAPG resulted in cell cycle arrest in G1 phase, downregulation of the expression of the cell cycle proteins cyclin D1, CDK4 and CDK6, an increase in the expression of cell cycle inhibitors (p21 and p27) and reduced cellular proliferation rates, whereas the opposite effects were observed with the overexpression of NCAPG. Taken together, these findings suggested that NCAPG affects cell proliferation via regulating the cell cycle, thereby providing a novel strategy for the treatment of gastric cancer with CDK4/6 inhibitors.

Clear cell renal cell carcinoma (ccRCC) is a common type of renal cancer (40). It has been revealed that the expression level of NCAPG is significantly upregulated in ccRCC (41). Li et al (42) showed that knocking down NCAPG resulted in a decrease in CDK1 expression, with the subsequent inhibition of cell proliferation, whereas overexpression of CDK1 partly reversed the reduction in the cell proliferation rate, suggesting that NCAPG is involved in the proliferation of ccRCC through its interaction with the CDK1 signalling pathway.

A previous study by Li et al (43) demonstrated that NCAPG is a key gene in LUAD, and a high expression level of NCAPG was shown to be strongly correlated with poor patient prognosis. Zhang et al (27) found that silencing NCAPG impeded the progression of NSCLC cells through inhibiting their proliferation, invasion and tumour growth, both in vitro and in vivo. Further investigation revealed that silencing NCAPG resulted in decreased expression levels of CDK4, CDK6 and cyclin D1, and an increased expression of p27 and p21, resulting in blockade of the cell cycle at G1 phase and the induction of apoptosis (27,44). Proline-rich protein 11 (PRR11) and spindle and kinetochore-associated 2 (SKA2) together form a classical head-to-head gene pair that serves an important role in tumour development (45). A previous study (46) demonstrated that, in NSCLC, NCAPG is able to interact with PRR11 and SKA2 to activate the Hedgehog (Hh) pathway, and the use of inhibitors of the Hh-regulated transcription factors GLI1 and GLI2 led to a marked reduction in the expression levels of PRR11, SKA2 and NCAPG. Taken together, these findings suggested that these three proteins are regulated by the Hh-GLI signalling pathway, thereby affecting the proliferation and migration rates of NSCLC cells.

Moura-Castro et al (47) reported that one of the mechanisms that may be associated with hyper-diploid acute lymphoblastic leukemia is an increased heterogeneity of the chromosome copy number due to the downregulation of NCAPG expression, which leads to the cohesion defect of sister chromosomes. It has been revealed that downregulation of NCAPG expression is also present in patients with multiple myeloma or acute myeloid leukemia, and that this may help to slow the proliferation rate and aggressiveness of cells associated with these types of cancer (22).

Association of NCAPG and cell stemness

Stemness, defined as the ability of a cell or tissue to self-renew and differentiate into multiple cell types, was originally identified in human embryonic stem cells, although subsequently it was found that pluripotent stem cells could be obtained from undifferentiated somatic cells by induction (48,49). In addition, certain normally differentiated cells have been shown to regain stem cell-like abilities in the event of loss of differentiation characteristics, and these are referred to as cancer stem cells (CSCs) (50,51). CSCs are capable of self-renewal and multidirectional differentiation, and exert an important role in promoting tumour progression, drug resistance and recurrence (52,53).

Through a biosignature study, Pan et al (54) demonstrated that NCAPG could be used as a biomarker for the characterization of bladder cancer stem cells. Subsequently, Li et al (55) found that, in brain low-grade gliomas (LGG), NCAPG was able to influence the E2F pathway and promote tumour recurrence through upregulating the expression level of the stemness indicator, aurora kinase A (AURKA). It has been found by Li et al (56) that expression of the circular RNA circNCAPG is higher in glioma stem cells compared with that in differentiated glioma cells, and that this is also associated with a worse prognosis. Ras response element binding protein 1 (RREB1) binds to circNCAPG and can regulate circNCAPG through the U2 nucleoprotein cofactor 65 kDa (U2AF65), thereby constituting a U2AF65/circNCAPG/RREB1 positive feedback loop. It was further found that RREB1 is able to promote the expression of proteins such as CD133, SRY-box transcription factor 2 (SOX2), Nanog and Oct4, whereas it had no direct regulatory effect on gene expression at the RNA level.

In addition, it has been identified that, in gastric cancer, high expression levels of NCAPG are associated with a higher stemness index and longer overall survival time compared with lower expression levels of NCAPG (57–59). Zhang et al (60) revealed that, in LUAD, NCAPG was positively correlated with the glycolysis marker genes HK2, PKM9 and LDHA. Upon knockdown of NCAPG, both the glycolytic level and the glycolytic capability of LUAD cells were found to be markedly reduced. Moreover, the expression levels of CD133, CD44 and Oct-4 were significantly increased when NCAPG was overexpressed, whereas the use of glycolysis inhibitors led to a reversal of the observed changes, suggesting that NCAPG promotes stemness of LUAD cells via activating the glycolytic pathway.

Association of NCAPG and immune infiltration

In tumour tissues, there are numerous other types of cells associated with the tumour microenvironment, such as normal stromal cells, immune cells and vascular endothelial cells (61,62). Interactions between tumour cells and the tumour microenvironment influence tumour development, and gaining an improved understanding of their roles should provide the key to unlocking a new era of tumour therapy (63,64).

Xu et al (65) found that NCAPG is one of the pivotal genes associated with M2-tumour-associated macrophage infiltration in prostate cancer, and that patients with high NCAPG expression had a poor prognosis. In addition, Xiang et al (57) found that, in stomach adenocarcinoma (STAD), increased macrophage expression levels with low expression of NCAPG led to the promotion of tumour progression and poor prognosis. NCAPG was positively correlated with the expression of certain immune checkpoint genes, including CD80, CTLA4, IDO1 and CD274, suggesting that STAD may be treated with corresponding immune checkpoint inhibitors. Li et al (55) found that the expression of NCAPG was upregulated in LGG and correlated with poor prognosis and immune infiltration (including an increased expression of CD8 T-cells, CD4 memory resting T-cells, macrophages and M1 macrophages). In NSCLC, a high expression of NCAPG was found to be associated with immune infiltration in which the levels of B cells, CD4 memory T cells, CD8 memory T cells, macrophages and natural killer (NK) T cells were reduced, thereby affecting the prognosis of NSCLC (9). Furthermore, it was shown by Guo and Zhu (24) that a high expression of NCAPG in HCC tissues was positively correlated with both immune cell infiltration (B cells, CD4 memory T cells, CD8 memory T cells, macrophages, neutrophils and dendritic cells) and the expression of associated molecular markers (CD19, IRF5, ITGAM and ITGAX), leading to poor prognosis. Interestingly, Xie et al (21) found that NCAPG was lowly expressed in BCC, and that this was significantly negatively correlated with NK cells and positively correlated with T regulatory cells, suggesting that NCAPG may fulfil an oncogene role in BCC, thereby providing guidance for new treatment strategies (Fig. 1).

Figure 1. Association between NCAPG and immune cells in glioma, basal cell carcinoma, lung cancer, hepatocellular carcinoma, stomach adenocarcinoma and prostate cancer. NCAPG, non-SMC condensin I complex subunit G; NK, natural killer; Treg, T regulatory.

NCAPG is involved in the regulation of tumour chemotherapy resistance

The tyrosine kinase Src is a proto-oncogene that exerts a key role in regulating cell proliferation, differentiation and metastasis (66,67). A previous study (68) revealed that the expression level of NCAPG is positively correlated with Src-associated genes; moreover, the expression level of NCAPG is increased in HER2+/trastuzumab-resistant BC, and this is closely correlated with shorter patient survival times and recurrence. Overexpression of NCAPG led to a markedly increased level of Src phosphorylation, whereas inhibition of Src using either specific inhibitors or shRNA resulted in reduced rates of cell proliferation, suggesting the important influence of NCAPG-dependent trastuzumab resistance. NCAPG overexpression promotes BC cell proliferation and resistance to apoptosis, and confers resistance to trastuzumab, whereas knockdown of NCAPG causes trastuzumab resistance to be restored, suggesting that the maintenance of low NCAPG expression may be more sensitive to the application of chemotherapeutic agents.

lncRNAs have been shown to fulfil important roles in tumour drug resistance (69–71). A study by Bao et al (72) found that, in LUAD, the mutation frequency of EGFR was increased with high expression of NCAPG compared with low NCAPG expression, and the IC50 value (the half-maximal inhibitory concentration) was found to be higher with the EGFR-tyrosine kinase inhibitor (EGFR-TKI) erlotinib, suggesting an association with resistance to EGFR-TKIs. Higher expression levels of NCAPG were also found in resistant patients with LUAD who were treated with either erlotinib or gefitinib. Using Ensembl database (73), it was revealed that NCAPG is able to potentially regulate the lncRNA AC099850.3; therefore, understanding the mechanism of the lncRNA AC099850.3-NCAGP signalling axis, and how this is associated with resistance to EGFR-TKIs, may provide a novel approach for the treatment of LUAD.

Mechanisms associated with signalling pathways and NCAPG in regulating tumour cells

NCAPG and the PI3K/AKT pathway

The PI3K/AKT pathway is an important cell signalling pathway that is involved in a variety of biological processes, including cell growth, proliferation, migration and invasion (74). A study by Gong et al (75) identified that NCAPG overexpression could both promote the phosphorylation and activation of PI3K and AKT and lead to the inhibition of FOXO4 phosphorylation, and that NCAPG was able to interact with PI3K, AKT and FOXO4 to activate PI3K/AKT/FOXO4 signalling, promote HCC cell proliferation and invasion and inhibit apoptosis; therefore, targeting and regulating NCAPG expression may provide a possible new avenue for the treatment of HCC. A study by Zhang et al (27) revealed that, in pancreatic adenocarcinoma, overexpression of NCAPG led to an increase in the phosphorylation levels of PI3K, AKT and GSK3β, whereas the use of AKT inhibitors caused a marked inhibition of the growth of lung cancer cells with high NCAPG expression.

miR-23b-3p is a cancer-associated biomarker that has been shown to be downregulated in colon cancer, which mediates tumour cell proliferation, migration and invasion (76,77). Li et al (78) demonstrated that miR-23b-3p was negatively correlated with NCAPG. Knockdown of NCAPG led to an inhibition of AKT phosphorylation and activation; moreover, NCAPG was found to interact with phosphorylated (p)-PI3K and p-AKT to negatively regulate apoptosis through influencing the miR-23b-3p/NCAPG/PI3K/AKT signalling pathway.

PTEN is a phosphatase that negatively regulates the PI3K/AKT pathway, and cancer may develop as a consequence of loss or mutation of the PTEN gene (79,80). Casein kinase 2 α1 (CKII) is a ubiquitous and highly conserved protein serine/threonine kinase that exerts an important role in cell cycle regulation and cell proliferation (81). Zhang et al (82) found that, in HCC, NCAPG is able to interact with CKII, thereby affecting PTEN expression. Upon overexpression of NCAPG, the levels of CKII, p-AKT and p-PTEN were found to be higher, resulting in the promotion of cell proliferation. Subsequently, the promotion of PTEN phosphorylation upon overexpression of NCAPG was found to be reversed with the use of CKII inhibitors, impairing cell proliferation. Taken together, these findings suggested that NCAPG inhibits PTEN expression through interaction with CKII, which in turn activates the PI3K/AKT pathway and promotes the proliferation of HCC cells.

NCAPG and the Wnt/β-catenin pathway

The Wnt pathway is an important signalling pathway that is involved in the regulation of cell proliferation, differentiation, apoptosis, stem cell self-renewal, tissue homeostasis and wound healing (83,84). Liu et al (85) showed that, in endometrial cancer, knockdown of NCAPG could inhibit tumour cell proliferation and promote cell apoptosis through inhibiting the expression of β-catenin. Zhang et al (86) demonstrated that, in pancreatic adenocarcinoma, overexpression of NCAPG led to an increase in the expression of vimentin, N-cadherin, Snail and Slug, and a decrease in the expression of E-cadherin, suggesting that overexpression of NCAPG may promote the EMT process in tumour cells. In addition, Shi et al (12) demonstrated that knockdown of NCAPG led to the inactivation of Wnt/β-catenin and EMT, which resulted in a marked inhibition in the migratory and invasion rates of colon cancer cells, thereby leading to the elimination of the accelerated cell migration and invasion rates that were caused by NCAPG overexpression. Moreover, it was revealed that NCAPG may be a downstream target of the Wnt/β-catenin signalling pathway, and that it is involved in cell proliferation, invasion, migration and EMT processes associated with colon cancer. Yang et al (87) reported that NCAPG interacts with chromobox protein homolog 3 (CBX3), which, in turn, regulates the expression of Wnt3a and β-linker proteins, whereas a deficiency of NCAPG led to an inhibition of cell invasion and the induction of apoptosis in colorectal cancer cells through its influence on the CBX3/NCAPG/Wnt pathway.

Li et al (88) revealed that NCAPG was highly expressed in oral cancer cells, and could directly bind to the oncogene miR-378a-3p; moreover, it was negatively regulated by miR-378a-3p. Knockdown of the NCAPG gene caused a marked inhibition of the GSK-3β/β-catenin pathway, suggesting that miR-378a-3p is able to regulate the GSK-3β/β-catenin pathway through affecting NCAPG expression.

NCAPG and the retinoblastoma (RB) tumour suppressor pathway

The RB pathway is a signalling pathway associated with cell cycle regulation, which serves an important role in cell proliferation and apoptosis (89,90). The core member of the RB pathway is the RB protein (pRb), a repressive transcription factor that inhibits cell cycle progression through binding to the transcription factor E2F (91,92). Xiao et al (4) showed that, in BC, the downregulation of NCAPG expression resulted in an increase in the level of poly(ADP-ribose) polymerase (PARP) protein, a decrease in the expression levels of pRb and cell cycle protein B1 and a marked inhibition of cell proliferation, suggesting that NCAPG may promote BC cell proliferation by regulating the RB pathway. In glioblastoma, Hou et al (26) revealed that NCAPG is able to interact with PARP1, a co-activator of E2F1, and that NCAPG is a downstream target gene of E2F1; moreover, a high expression of NCAPG positively regulates the E2F1 pathway.

NCAPG and the p53 pathway

p53 is an important oncogene that has significant roles in the regulation of cell cycle, senescence and apoptosis (93,94). Dong et al (95) identified a number of miRNAs (such as miR-101-3p, miR-195-5p, miR-214-3p and miR-944) that serve to reduce NCAPG expression to promote BC development, and these are enriched in the p53 signalling pathway. In addition, it was observed that knockdown of NCAPG gene expression resulted in a significant decrease in the expression level of CDC25C, which acts as a direct target of p53 transcription factor and cell cycle arrest in G2/M phase, further emphasizing its function as an oncogene. Taking all these findings into consideration, it has been proposed that NCAPG may influence the p53 signalling pathway via regulating the expression of CDC25C.

NCAPG and the NF-κB pathway

NF-κB represents a class of transcription factors that fulfill key roles in several biological processes, including inflammation, immune response and cell growth (96,97). A previous study by Swindell et al (98) identified NCAPG as a potential NF-κB target gene. In bladder cancer (99), knockdown of NCAPG was shown to result in a lower degradation rate of IκBα and inhibition of the NF-kB pathway in a dose-dependent manner. Knockdown of NCAPG also resulted in downregulation of the expression of NF-κB downstream genes, including TNFα, inhibitor of apoptosis 2 (IAP2), inhibitor of NF-κB kinase regulatory subunit γ (IKBKG), interleukin (IL)-2RB, IL-2RG, interferon regulatory factor 1 (IRF1) and TNFAIP3 interacting protein 1 (TNIP1), thereby attenuating cell proliferation. It has been suggested that NCAPG promotes bladder cancer progression through regulating the NF-κB signalling pathway (Fig. 2).

Figure 2. Mechanisms via which NCAPG regulates malignant tumour development through the PI3K/AKT/GSK-3β, Wnt/β-catenin and NF-κB pathways. NCAPG, non-SMC condensin I complex subunit G.

NCAPG and the signal transducer and activator of transcription 3 (STAT3) signalling pathway

STAT3 is a transcription factor that fulfils important roles in tumour cell proliferation, metastasis, invasion and immunosuppression (100,101). A previous study by Li et al (102) found that, in triple-negative BC, knockdown of NCAPG resulted in a significant decrease in the expression of p-EGFR, p-JAK1 and p-STAT3, although the inhibitory effect of knockdown of NCAPG on p-STAT3 could be reversed by using agonists of the EGFR and JAK/STAT3 signalling pathways, accompanied by an increase in cell proliferation, invasion and migration and a decrease in apoptosis. NCAPG was demonstrated to affect cell proliferation, invasion, migration and apoptosis through influencing the EGFR/JAK/STAT3 signalling pathway. Jiang et al (68) revealed that overexpression of NCAPG led to an increase in the transcriptional activity and phosphorylation level of STAT3, as well as increasing the expression level of the downstream factors of STAT3 signalling, cytosolic protein D1 and BCL2, whereas inhibition of NCAPG elicited the opposite results. Taken together, these results suggested that NCAPG may mediate BC cell proliferation and exert its anti-apoptotic effects through activation of the Src/STAT3 signalling pathway.

NCAPG and the transforming growth factor β (TGF-β) pathway

TGF-β is an important extracellular signalling molecule that has a key role in physiological processes, including cell growth, differentiation and migration, apoptosis, immunity and EMT (103,104). Wu et al (23) found that the expression of p-Smad2 and p-Smad3 in the TGF-β signalling pathway was increased upon overexpression of NCAPG, leading to the promotion of cell proliferation, invasion, migration and EMT. Subsequently, upon overexpression of NCAPG, the use of an inhibitor of the TGF-β signalling pathway effectively reversed the effects mediated on the EMT process and the proliferative, migratory and invasive capabilities of LUAD cells. Li et al (56) demonstrated that circNCAPG is highly expressed in glioma stem cells, where it interacts with the RNA-binding protein U2AF65. It was further found that circNCAPG binds to RREB1, promoting RREB1 entry into the nucleus and activating the TGF-β1 pathway. It was therefore suggested that RREB1 promotes glioma stem cell proliferation, invasion and maintenance of self-renewal through promoting the expression of U2AF65, enhancing the stability of circNCAPG and forming the U2AF65/circNCAPG/RREB1 positive feedback pathway.

Conclusions

Intracellularly, increased expression of NCAPG promotes cell proliferation by facilitating the transition from G1 to S and G2/M phases. NCAPG can also affect the proliferation, apoptosis and EMT of tumour cells through multiple signalling pathways, including PI3K/AKT, Wnt, RB, p53, STAT3 and TGF-β, promoting tumour development and progression. In addition, it is important to focus on the fact that NCAPG is able to promote the maintenance of stem cell properties by affecting the Wnt/β-catenin pathway. Extracellularly, high expression of NCAPG was associated with enhanced invasiveness and migration of tumour cells. Furthermore, NCAPG may help tumour cells evade the immune system by affecting immune cells in the tumour microenvironment. In conclusion, NCAPG, as a cell cycle regulatory protein, promotes cell proliferation not only inside the cell by affecting the cell cycle and cell stemness, but also outside the cell by affecting the tumour microenvironment to promote tumour invasion and metastasis. Continuing research and in-depth studies on the function and underlying molecular mechanisms of NCAPG should lay the foundation for the discovery of novel antitumour drug targets, and the realization of precise and personalized tumour therapies.

Acknowledgements

Not applicable.

Funding

The present study was supported by the Affiliated Hospital of Zunyi Medical University [grant no. Institution (2015) 34], the Guizhou Provincial Department of Science and Technology [grant no. Qiankehe LH Zi (2014) 7573], the Affiliated Hospital of Zunyi Medical University [grant no. Institution (2016) 45] and the Collaborative Innovation Center of Chinese Ministry of Education (grant no. 2020-39).

Availability of data and materials

Not applicable.

Authors' contributions

RL and DW drafted the manuscript and contributed equally to the study. HY and LP participated in the literature search and analysis of the data to be included in the review. XL and FY were involved in the design of the study and assisted in the preparation of the figures. RZ edited and revised the manuscript. All authors have read and approved the final version of the manuscript. Data authentication is not applicable.

Ethics approval and consent to participate

Not applicable.

Patient consent for publication

Not applicable.

Competing interests

The authors declare that they have no competing interests.

References