Open AccessmiR‑494‑3p promotes the progression of endometrial cancer by regulating the PTEN/PI3K/AKT pathway
Author(s) -
Lichao Zhu,
Xiaoyan Wang,
Tao Wang,
Wenwen Zhu,
Xinge Zhou
Publication year - 2018
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2018.9649
Subject(s) - pten , tensin , pi3k/akt/mtor pathway , cancer research , protein kinase b , downregulation and upregulation , phosphatase , microrna , biology , cancer , oncogene , phosphoinositide 3 kinase , cell growth , cell cycle , chemistry , microbiology and biotechnology , signal transduction , phosphorylation , gene , biochemistry , genetics
MicroRNAs (miRs) are essential regulators in the development and progression of cancer. The role of miR-494-3p in endometrial cancer (EC) has not yet been investigated. In the present study, the expression levels of miR‑494‑3p were significantly upregulated in EC tissues compared with adjacent normal tissues. Furthermore, upregulation of miR‑494‑3p in patients with EC indicated poorer prognosis; miR‑494‑3p overexpression significantly promoted the proliferation, migration and invasion of HHUA and JEC cells in vitro. Consistently, inhibition of miR‑494‑3p in HHUA cells significantly suppressed tumor growth in vivo in a xenograft model. Additionally, phosphatase and tensin homolog (PTEN) was revealed to be a direct target of miR‑494‑3p in EC cells. Furthermore, overexpression of miR‑494‑3p inhibited PTEN expression and consequently activated the downstream phosphoinositide 3‑kinase/protein kinase B (PI3K/AKT) signialing pathway. Restoration of PTEN or inhibition of PI3K/AKT pathway also abolished miR‑494‑3p‑mediated proliferation, migration and invasion of HHUA and JEC cells. In summary, the results of the present study revealed the importance of the miR‑494‑3p/PTEN/PI3K/AKT axis in the progression of EC, which may provide novel insight into potential therapeutic targets for the treatment of EC.