LncRNA UCA1 inhibits proliferation and promotes apoptosis of cervical cancer cells by regulating β-catenin/TCF-4.

Abstract

The aim of this study was to explore the regulatory effect of long non-coding ribonucleic acid (lncRNA) urothelial carcinoma antigen 1 (UCA1) on the proliferation and apoptosis of HeLa cells and to elucidate its potential regulatory mechanism. HeLa cells were cultured in vitro and randomly divided into three groups, including blank control group (Control group), lncRNA UCA1 negative control (NC) group, and lncRNA UCA1 interference group [lncRNA UCA1 small interfering RNA (siRNA) group]. The expression level of lncRNA UCA1 in HeLa cells was detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Methyl thiazolyl tetrazolium (MTT) assay was performed to determine the effect of lncRNA UCA1 on the proliferation of HeLa cells. The effect of lncRNA UCA1 on the apoptosis of HeLa cells was determined via Hoechst 33258 staining assay and flow cytometry. In addition, qRT-PCR and Western blotting were employed to measure the messenger RNA (mRNA) and protein expression levels of β-catenin and TCF-4 in HeLa cells, respectively. There were no statistically significant differences in the proliferation and apoptosis of HeLa cells as well as the mRNA and protein levels of β-catenin and TCF-4 in HeLa cells between Control group and lncRNA UCA1 NC group (p>0.05). In comparison with lncRNA UCA1 NC group, lncRNA UCA1 siRNA group exhibited overtly reduced proliferation, enhanced apoptosis rate of HeLa cells and down-regulated mRNA and protein levels of β-catenin and TCF-4 in HeLa cells (p<0.05). LncRNA UCA1 inhibits proliferation and promotes the apoptosis of HeLa cells. Furthermore, its mechanism of action may be related to the inhibition on the β-catenin/TCF-4 signaling pathway.