LncRNA BCYRN1/miR-490-3p/POU3F2, served as a ceRNA network, is connected with worse survival rate of hepatocellular carcinoma patients and promotes tumor cell growth and metastasis

Abstract

Abstracts Backgrounds LncRNA Brain Cytoplasmic RNA 1 (BCYRN1) has been certified to modulate cancer cells growth and aggressiveness in several tumors. However, research about function of BCYRN1 in hepatocellular carcinoma (HCC) is limited. Therefore, our research intends to explore the function of BCYRN1 in HCC. Methods HepG2 and BEL-7402 cell lines were employed for later function experiments. Differently expression levels of BCYRN1, miR-490-3p, and POU class 3 homeobox 2 (POU3F2) were determined on the base of TCGA dataset including 375 HCC patients and 50 normal. 370 cases of patients, which have fairly complete clinical data, were utilized for survival analysis of BCYRN1, miR-490-3p, or POU3F2 by Kaplan–Meier method. Relative expression pattern of BCYRN1 was examined by quantitative real time polymerase chain reaction (qRT-PCR), and relative expression level of POU3F2 was assessed by qRT-PCR and western blot. Cell biological behaviors were analyzed by cell counting kit-8, cloning formation, and transwell assays. Bioinformatics software and dual luciferase assay were applied to predict and confirm the targeted relationship between BCYRN1 and miR-490-3p, as well as miR-490-3p and POU3F2. Further associations among BCYRN1, miR-490-3p, and POU3F2 were analyzed by rescue assays. Results Our results exhibited that BCYRN1 was over expressed in HCC samples, which was connected with unfavorable prognosis in HCC patients. In addition, a series of experiments exhibited that overexpression of BCYRN1 significantly expedited HCC cells growth, clone formation, and movement abilities, and vice versa. Moreover, targeted relationships between BCYRN1 and miR-490-3p, as well as miR-490-3p and POU3F2 were affirmed by dual luciferase assay. Furthermore, POU3F2 expression was negatively connected with the expression of miR-490-3p and positively associated with BCYRN1 expression. Whilst, either overexpression of miR-490-3p or knockdown of POU3F2 could remarkably inhibit the increasing trends of proliferation, clone formation, invasion, and migration abilities induced by BCYRN1 in HCC cells. Conclusions BCYRN1, served as a competing endogenous RNA, up-regulated the expression of POU3F2 to promote the development of HCC through sponging miR-490-3p, supplying novel molecular targets and underlying prognostic biomarkers for HCC therapy.