miR‑494‑3p promotes the progression of endometrial cancer by regulating the PTEN/PI3K/AKT pathway.

Abstract	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.
Authors	Lichao Zhu, Xiaoyan Wang, Tao Wang, Wenwen Zhu, Xinge Zhou
Journal	Molecular medicine reports (Mol Med Rep) Vol. 19 Issue 1 Pg. 581-588 (01 2019) ISSN: 1791-3004 [Electronic] Greece
PMID	30431102 (Publication Type: Journal Article)
Chemical References	MIRN494 microRNA, human MicroRNAs Phosphatidylinositol 3-Kinases Proto-Oncogene Proteins c-akt PTEN Phosphohydrolase PTEN protein, human
Topics	Animals Apoptosis Cell Movement Cell Proliferation Disease Progression Endometrial Neoplasms (genetics, metabolism, pathology) Female Gene Expression Regulation, Neoplastic Humans Mice Mice, Inbred BALB C Mice, Nude MicroRNAs (genetics) Middle Aged PTEN Phosphohydrolase (genetics, metabolism) Phosphatidylinositol 3-Kinases (genetics, metabolism) Proto-Oncogene Proteins c-akt (genetics, metabolism) Signal Transduction Tumor Cells, Cultured Xenograft Model Antitumor Assays

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