Open AccessMicroRNA-296-5p downregulated AKT2 to inhibit hepatocellular carcinoma cell proliferation, migration and invasion
Author(s) -
Xiaoli Ma,
Zhuang Baoxiang,
Wentao Li
Publication year - 2017
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.2017.6701
Subject(s) - oncogene , akt2 , cancer research , molecular medicine , carcinogenesis , hepatocellular carcinoma , microrna , metastasis , cell cycle , malignancy , cell growth , cell , tumor progression , biology , cancer , oncology , medicine , cell migration , apoptosis , akt1 , gene , protein kinase b , biochemistry , genetics
Hepatocellular carcinoma (HCC) is the fifth most common malignancy in men, and the seventh in women worldwide. Despite development in the therapy of HCC, the prognosis of HCC patients remains poor. Therefore, it is of great significance to explore the molecular mechanism underlying HCC progression, and investigate novel therapeutic strategies for the treatments of HCC. MicroRNAs (miRs) are known to be involved in the pathogenesis of HCC. The present study aimed to investigate the expression patterns and potential roles of miR‑296‑5p in HCC. Results revealed that miR‑296‑5p was frequently downregulated in HCC tissue samples and cell lines. Additionally, reduced miR‑296‑5p expression levels were correlated with tumor size, TNM stage and metastasis in HCC. Gain‑of‑function demonstrated that miR‑296‑5p inhibited HCC cell proliferation, migration and invasion in vitro. Furthermore, AKT2 was identified as a novel direct and functional target of miR‑296‑5p in HCC. These findings indicated that miR‑296‑5p/AKT2 axis serves important roles in HCC carcinogenesis and progression, and miR‑296‑5p/AKT2 based target therapy hampers HCC tumor growth and metastasis.