STAT1-Induced Upregulation lncRNA LINC00958 Accelerates the Epithelial Ovarian Cancer Tumorigenesis by Regulating Wnt/β-Catenin Signaling.

Min Xie,Pin-Pin Wang,Qi Fu,Yu-Lan Cui,Fu Wang

doi:10.1155/2021/1405045

Abstract

Background Growing studies have demonstrated that long noncoding RNAs (lncRNAs) play important roles in tumor progression. In this study, we aimed to explore the potential roles of lncRNA LINC00958 (LINC00958) and its biological functions in epithelial ovarian cancer (EOC). Methods The expression of LINC00958 in 11 cases of EOC and adjacent nontumor specimens and five cell lines was detected by qRT-PCR. CCK-8, colony formation, and flow cytometry assays were conducted to study the cell viabilities of EOC cells. Wound scratch and transwell analyses were carried out for the examination of cell invasion and migration of EOC cells. The targeting associations between LINC00958 and STAT1 were demonstrated by ChIP analyses combined with luciferase reporter assays. The related proteins of Wnt/β-catenin signaling were determined using RT-PCR. Results Higher levels of LINC00958 were observed in EOC tissues and cell lines. Our data also revealed that high LINC00958 expression was partly induced by STAT1. Functionally, knockdown of LINC00958 suppressed the proliferation, migration, and invasion of EOC cells. Mechanistic investigation showed that the inhibitory effect of LINC00958 knockdown on EOC cells was mediated by the Wnt/β-catenin signaling. Conclusion Our findings suggested that STAT1-induced overexpression of LINC00958 promoted EOC progression by modulating Wnt/β-catenin signaling.

Highlights

Ovarian cancer is the 8th most common gynaecological cancer worldwide and regarded as one of the most frequent tumorassociated deaths in females, with a growing incidence in China [1, 2]
In order to demonstrate the above findings, we performed RT-PCR in epithelial ovarian cancer (EOC) tissues and normal tissues from 11 EOC patients in our hospital: the results showed that LINC00958 levels in EOC tissues were distinctly higher than those in normal specimens (p < 0:01, Figure 1(b))
SiContrsoilLnc-1siLnc-2 SKOV3 (b) cyclin D1 c-myc and migration of EOC cells by modulating miR-338-3p [24]. These findings suggested that further exploration of potential functions of long noncoding RNAs (lncRNAs) may provide novel insights that could help the improvement of early diagnosis, effective therapies, and prognosis prediction

Summary

Background

Growing studies have demonstrated that long noncoding RNAs (lncRNAs) play important roles in tumor progression. We aimed to explore the potential roles of lncRNA LINC00958 (LINC00958) and its biological functions in epithelial ovarian cancer (EOC). The expression of LINC00958 in 11 cases of EOC and adjacent nontumor specimens and five cell lines was detected by qRT-PCR. CCK-8, colony formation, and flow cytometry assays were conducted to study the cell viabilities of EOC cells. Wound scratch and transwell analyses were carried out for the examination of cell invasion and migration of EOC cells. The related proteins of Wnt/β-catenin signaling were determined using RT-PCR. Knockdown of LINC00958 suppressed the proliferation, migration, and invasion of EOC cells. Mechanistic investigation showed that the inhibitory effect of LINC00958 knockdown on EOC cells was mediated by the Wnt/β-catenin signaling. Our findings suggested that STAT1induced overexpression of LINC00958 promoted EOC progression by modulating Wnt/β-catenin signaling

Introduction

Materials and Methods

Results

Discussion

Conclusion

Conflicts of Interest