Long non-coding RNA PTAR inhibits apoptosis but promotes proliferation, invasion and migration of cervical cancer cells by binding miR-101

In this study, the expression of PTAR in cervical cancer tissues and cells was quantified by real-time PCR. Then, the roles of PTAR in HeLa cell proliferation and cell cycle were analyzed by a CCK-8 assay and flow cytometry, respectively.The effects of PTAR on cell migration and invasion were checked by Transwell and wound healing assays.The effect of PTAR on HeLa cell apoptosis was analyzed using annexin V/FITC staining. Finally, the interaction between PTAR and miR-101 in uterine cancer was verified through a dual-luciferase reporter assay and correlation analysis. The results showed that PTAR expression was aberrantly ascended in cervical cancer tissues and cell lines (Caski, SW756, SiHa, C33A and HeLa cells). Overexpressed PTAR could promote cell proliferation, migration and invasion in HeLa cells, which were suppressed by PTAR knockdown. Moreover, cell cycle progression stalled at the G1-G0 phase could be released with PTAR overexpression. The transfection of a PTAR vector inhibited apoptosis, while si-PTAR transfection increased apoptosis. Furthermore, PTAR could act as an endogenous sponge by directly binding to miR-101 and downregulating miR-101 expression. In conclusion, lncRNAPTAR plays a vital role and may be an effective target for the diagnosis and therapy of cervical cancer.

Automated summary

The study demonstrated that an aberrant upregulation of PTAR in cervical cancer tissues and cell lines promotes proliferation, migration, and invasion of HeLa cells, while inhibiting apoptosis and downregulating miR-101 expression through direct binding. These findings suggest that PTAR plays a crucial role and may serve as a promising target for cervical cancer diagnosis and therapy.