Long non‐coding RNA FEZF1‐AS1 induced progression of ovarian cancer via regulating miR‐130a‐5p/SOX4 axis. Issue 7 (5th March 2020)

• Record Type: Journal Article
• Authors: Sun, Ziqian; Gao, Shouyang; Xuan, Lili; Liu, Xiaojun
• Is Part Of: Journal of cellular and molecular medicine. Volume 24:Issue 7(2020)
• Page Start: 4275
• Page End: 4285
• Publication Date: 2020-03-05
• Subjects: epithelial ovarian cancer -- FEZF1 antisense RNA 1 (FEZF1‐AS1) -- invasion -- migration -- miR‐130a‐5p -- proliferation; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.15088
• Languages: English
• ISSNs: 1582-1838

Abstract

Abstract: Emerging studies have revealed the critical role of long non‐coding RNAs (lncRNAs) in epithelial ovarian cancer (EOC) development and progression. Till now, the roles and potential mechanisms regarding FEZF1 antisense RNA 1 (FEZF1‐AS1) within ovarian cancer (OC) remain unclear. The objective of this study was to uncover the biological function and the underlying mechanism of LncRNA FEZF1‐AS1 in OC progression. FEZF1‐AS1 expression levels were studied in cell lines and tissues of human ovarian cancer. In vitro studies were performed to evaluate the impact of FEZF1‐AS1 knock‐down on the proliferation, invasion, migration and apoptosis of OC cells. Interactions of FEZF1‐AS1 and its target genes were identified by luciferase reporter assays. Our data showed overexpression of FEZF1‐AS1 in OC cell lines and tissues. Cell migration, proliferation, invasion, wound healing and colony formation were suppressed by silencing of FEZF1‐AS1. In contrast, cell apoptosis was promoted by FEZF1‐AS1 knock‐down in vitro. Furthermore, online bioinformatics analysis and tools suggested that FEZF1‐AS1 directly bound to miR‐130a‐5p and suppressed its expression. Moreover, the inhibitory effects of miR‐130a‐5p on the OC cell growth were reversed by FEZF1‐AS1 overexpression, which was associated with the increase in SOX4 expression. In conclusion, our results revealed that FEZF1‐AS1 promoted the metastasis and proliferation of OC cells by targeting miR‐130a‐5p and its downstream SOX4 expression.