Open AccessmiR ‐744‐5p inhibits cellular proliferation and invasion via targeting ARF1 in epithelial ovarian cancer
Author(s) -
Zhao LaiGang,
Wang Jiao,
Li Jin,
Li QinFen
Publication year - 2020
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1002/kjm2.12253
Subject(s) - cancer research , western blot , cell growth , epithelial ovarian cancer , microrna , medicine , ovarian cancer , cell , cell migration , cancer , biology , gene , biochemistry , genetics
miR‐744‐5p has been demonstrated to play an important role in cancer progression. However, the functions of miR‐744‐5p in epithelial ovarian cancer (EOC) are not well clarified. In this study, our aim was to investigate the role of miR‐744‐5p and its underlying molecular mechanism in cell progression of EOC. EOC clinical tissues and matched adjacent ovarian epithelial tissues were collected from 18 patients. Tissues and cell lines were analyzed by qPCR or Western blot to investigate the expression of miR‐744‐5p and ARF1 in EOC. Cell proliferative capacity was assessed by CCK8 and colony formation assays. Wound healing and transwell assays were performed to evaluate cell migration and invasion. The potential binding relation between miR‐744‐5p and IRF1 was demonstrated by dual luciferase report assay. The results showed that expression of miR‐744‐5p was low in EOC clinical tissues and cells. Overexpression of miR‐744‐5p inhibited proliferation, migration, and invasion of EOC cells. Further mechanistic study identified that ARF1 is a target of miR‐744‐5p, which is negatively correlated with the expression of miR‐744‐5p, and overexpression of ARF1 could reverse the inhibition of miR‐744‐5p on the proliferation, migration, and invasion of EOC cells. Taken together, our results indicated that miR‐744‐5p attenuated EOC progression via targeting IRF1, providing potential guidance for the clinical treatment of ovarian cancer.