Long non-coding RNA PVT1 promotes the proliferation, migration and EMT process of ovarian cancer cells by regulating CTGF.

Ovarian cancer remains one of the most common gynecological malignancies with a poor prognosis. The present study investigated the roles of long non-coding RNA plasmacytoma variant translocation 1 (lncRNA PVT1) in the regulation of the malignant phenotype of ovarian cancer cells, including cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT). SKOV3 and CAOV3 cells were transfected with small interfering RNA (siRNA) targeting lncRNA PVT1 (si-PVT1) or control siRNA and the si-PVT1 transfected cells were co-cultured with recombinant human connective tissue growth factor (rhCTGF). The proliferation, migration and invasion abilities of the cells were examined via Cell Counting Kit-8, colony formation, wound-healing and Transwell assays. The relative expression levels of lncRNA PVT1, CTGF, E-cadherin and vimentin were analyzed using reverse transfection-quantitative polymerase chain reaction, and western blotting was employed to detect the protein levels of CTGF, E-cadherin and vimentin. The expression of lncRNA PVT1 was significantly reduced in SKOV3 and CAOV3 cells following transfection with si-PVT1. In addition, the proliferation, migration and invasion abilities of SKOV3 and CAOV3 cells were repressed following lncRNA PVT1 knockdown. The knockdown of lncRNA PVT1 also reduced the expression of CTGF and vimentin, and increased the expression of E-cadherin. The changes in the proliferation, migration and invasion of the cells induced by transfection with si-PVT1 were partially attenuated in the presence of rhCTGF. Furthermore, co-culture with rhCTGF reversed the si-PVT1-induced changes in the expression of EMT-associated proteins. In conclusion, lncRNA PVT1 promotes the proliferation, migration, invasiveness and EMT process of ovarian cancer cells, and CTGF contributes to the effect of lncRNA PVT1.