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

Abstract

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.

Role of STAT3 in cancer cell epithelial‑mesenchymal transition (Review)

“…The lncRNA, PVT1, has been shown to facilitate EMT by physically interacting with activated STAT3, which then enhances STAT3 binding to the Slug promoter, increasing Slug expression to facilitate EMT (54). Indeed, several studies have revealed that PVT1 is an EMT inducer (52,53,(184)(185)(186)(187). Furthermore, STAT3 was also shown to upregulate PVT1 expression through binding to its promoter (14) and therefore, PVT1 and STAT3 form a positive regulatory loop to enhance cancer progression.…”

“…Plasmacytoma variant translocation 1 (PVT1) is a well-studied lncRNA that is located at the 8q24.21 region near the c-Myc oncogene. PVT1 is upregulated by copy number amplification and is able to promote cancer progression ( 52 , 53 ). Zhao et al ( 54 ) showed that PVT1 enhances STAT3 recruitment to the Slug promoter, and transcriptionally enhances Slug expression in gastric cancer.…”

The Role of EMT-Related lncRNAs in Ovarian Cancer

“…The authors suggested that this lncRNA promotes OC cell proliferation, metastasis, and EMT via sponging miR-140-3p and thus increases SNAI2 expression [ 67 ]. Plasmacytoma-variant translocation 1 (PVT1) enhanced the proliferative and migrative potential of OC cells through the modulation of the expression of connective tissue growth factor (CTGF), which in turn also promotes the EMT process [ 69 ]. Moreover, SNHG17 knockdown was found to repress EMT in OC cells via the regulation of miR-485p/AKT1 axis [ 71 ].…”