LncRNA ROR promotes proliferation of endometrial cancer cells via regulating Notch1 pathway.

Abstract

The aim of this study was to investigate the effects of long non-coding ribonucleic acid regulator of reprogramming (lncRNA ROR) on the proliferation and apoptosis of endometrial cancer (EC) cells, and to explore its possible underlying mechanism. The expression levels of lncRNA ROR and Notch1 in EC tissues were detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The changes in Notch1 protein were detected via Western blotting. Subsequently, the regulatory mechanism of lncRNA ROR on Notch1 was analyzed using Luciferase reporter gene assay. Moreover, the changes in cell proliferation and apoptosis were determined through cell counting kit-8 (CCK-8) assay and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, respectively. Both lncRNA ROR and Notch1 were highly expressed in EC tissues (p<0.05). After overexpression of lncRNA ROR, HEC-1A cells had significantly enhanced proliferation (p<0.05) and weakened apoptosis (p<0.05). Meanwhile, the mRNA and protein levels of Notch1 rose remarkably compared with those in control group (p<0.05). Luciferase reporter gene assay revealed that lncRNA ROR could bind to the Notch1 regulatory factor miR-34a and inhibit its activity. LncRNA ROR regulates the proliferation and apoptosis of EC cells via promoting the expression of Notch1 protein.