MicroRNA‑494 promotes the proliferation and migration of human glioma cancer cells through the protein kinase�B/mechanistic target of rapamycin pathway by phosphatase and tensin homolog expression
Author(s) -
Kun Han,
Li Zhao,
Peng Sun
Publication year - 2018
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2018.6823
Subject(s) - tensin , pten , pi3k/akt/mtor pathway , glioma , cancer research , protein kinase b , biology , cell growth , cancer cell , mechanistic target of rapamycin , cell cycle , cancer , microbiology and biotechnology , signal transduction , biochemistry , genetics
The aim of the present study was to analyze the possible association between microRNA‑494 (miR‑494) and cell proliferation in glioma cancer. Firstly, the expression of miR‑494 was revealed to be upregulated in patients with glioma, compared with the normal group. Next, anti‑miR‑494 mimics were used to decrease the expression of miR‑494 in glioma cancer cells, which subsequently induced apoptosis, and inhibited cell growth and migration. Downregulation of miR‑494 expression induced phosphatase and tensin homolog (PTEN) and suppressed the protein kinase B/mechanistic target of rapamycin pathway (Akt/mTOR) pathway in glioma cancer cells. By contrast, overexpression of miR‑494 by miR‑494 mimics promoted cell growth and migration, and suppressed the apoptosis of glioma cancer via the Akt/mTOR pathway by PTEN expression. Furthermore, a PTEN inhibitor was used to attenuate the function of miR‑494 in glioma cancer autophagy through Akt/mTOR pathway. The promotion of PTEN promoted the function of anti‑miR‑494 on glioma cancer cell growth through Akt/mTOR pathway. Collectively, these results demonstrate that the effect of miRNA‑494 on the proliferation and migration glioma cancer cells was mediated through Akt/mTOR pathway by PTEN expression.
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