Open AccessMicroRNA‐1258, regulated by c‐Myb, inhibits growth and epithelial‐to‐mesenchymal transition phenotype via targeting SP1 in oral squamous cell carcinoma
Author(s) -
Zhang Hua,
Jiang Sui,
Guo Longbin,
Li Xi
Publication year - 2019
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.14189
Subject(s) - cancer research , microrna , cell growth , epithelial–mesenchymal transition , pi3k/akt/mtor pathway , biology , mapk/erk pathway , protein kinase b , western blot , cell culture , cancer , signal transduction , microbiology and biotechnology , metastasis , gene , genetics
The biological function and underlying mechanism of miR‐1258 has seldom been investigated in cancer progression, including in oral squamous cell carcinoma (OSCC). In the current study, we revealed that the expression level of miR‐1258 was significantly down‐regulated in OSCC tissues and cell lines. Restoration of miR‐1258 decreased OSCC cell growth and invasion. The luciferase and Western blot assays revealed that SP1 protein was a downstream target of miR‐1258. Overexpression of SP1 dismissed miR‐1258’s effect on cell growth and invasion. We also revealed that c‐Myb inhibited miR‐1258 by directly binding at its promoter. In addition, miR‐1258 inhibited PI3K/AKT and ERK signalling pathway activity. Taken together, these findings demonstrated that miR‐1258 may function as a tumour‐suppressive micorRNA in OSCC and suggested that miR‐1258 may be a potential therapeutic target for OSCC patients.