CBX7 is involved in the progression of cervical cancer through the ITG3/TGF1/AKT pathway

The chromobox protein homolog 7 (CBX7) serves a tumor-suppressive role in human malignant neoplasias. The downregulation of CBX7 is associated with the poor prognosis and aggressiveness of various human cancers. However, the biological functions and underlying mechanisms of CBX7 in cervical cancer remain unclear. The present study investigated the role and mechanism of CBX7 in cervical cancer. Lentivirus and siRNA were used to construct cervical cancer cells with stable CBX7 knockdown and SiHa xenograft models. The cell growth, migration, invasion and apoptosis were observed through in vivo and in vitro experiments. The expression levels of CBX7, integrin beta 3 (ITG beta 3), transforming growth factor beta 1 (TGF beta 1), phosphatidylinositol-3-kinase (PI3K), AKT, E-cadherin (E-cad) and vimentin (VIM) were detected by western blot analysis and reverse transcription-quantitative PCR. The correlation between CBX7 and these genes was analyzed. TGF beta 1 was also silenced through shRNA in cells with stable CBX7 knockdown to detect its effect on cell growth, invasion and apoptosis, and on pathway-related gene expression. It was revealed that knockdown of CBX7 promoted the proliferation, migration, and invasion of cervical cancer cells, and inhibited apoptosis. In addition, CBX7 knockdown promoted tumor growth in vivo. Correlation analysis demonstrated that CBX7 was negatively correlated with ITG beta 3, TGF beta 1, PI3K, AKT, phosphorylated AKT and VIM, but positively correlated with E-cad. Moreover, the knockdown of TGF beta 1 reversed the promotion of cell proliferation and inhibition of apoptosis induced by CBX7 knockdown and attenuated the increase of ITG beta 3, TGF beta 1, PI3K, AKT and VIM caused by CBX7 knockdown. In conclusion, the findings of the present study indicated that the downregulation of CBX7 enhances cell migration and invasion while inhibiting cell apoptosis in cervical cancer by modulating the ITG beta 3/TGF beta 1/AKT signaling pathways.