Y.C. Zhao and Y. Li

Author information

Department of Obstetrics and Gynecology, The Second People’s Hospital of Lanzhou, Lanzhou, Gansu, P.R. China

Abstract

Long non-coding RNA small nucleolar RNA host gene 7 (lncRNA SNHG7) and microRNA-34a (miR-34a) have been implicated in ovarian cancer (OC) development. Furthermore, the binding of SNHG7 to miR-34a is widely recognized in numerous cancers. Therefore, our research intended to explore the specific mechanism of SNHG7 and miR-34a in OC. SNHG7, miR-34a, and endothelial differentiation gene (EDG) 4 expression in harvested OC tissues and cells were measured by RT-qPCR. Dual-luciferase reporter gene assay and RIP assay were implemented to assess the binding of SNHG7 to miR-34a, and of miR-34a to EDG4. Gain- and loss-of-function assays were implemented in OC cells, followed by Scratch test and Transwell assay of cell migration and invasion, respectively. The epithelial-mesenchymal transition (EMT) and the PI3K/AKT pathway-related proteins were measured by Western blot analysis. SNHG7 and EDG4 were overexpressed, but miR-34a was poorly expressed in OC tissues and cells. miR-34a bound to SNHG7 and targeted directly EDG4, and SNHG7 activated the PI3K/AKT pathway in OC cells. Furthermore, SNHG7 or EDG4 silencing, miR-34a overexpression, or PI3K/AKT pathway bluntness diminished OC cell invasion, migration, and EMT. Collectively, SNHG7 downregulation repressed EMT of OC cells via miR-34a-targeted EDG4 and the PI3K/AKT pathway.

Keywords:

Ovarian cancer, Long non-coding RNA SNHG7, microRNA-34a, EDG4, PI3K/AKT pathway, Epithelial-mesenchymal transition

Publication type

Journal Article

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