Open AccessmiR‐335 inhibited cell proliferation of lung cancer cells by target Tra2β
Author(s) -
Liu Jian,
Bian Tingting,
Feng Jia,
Qian Li,
Zhang Jianguo,
Jiang Daishan,
Zhang Qing,
Li Xiaoli,
Liu Yifei,
Shi Jiahai
Publication year - 2018
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.13452
Subject(s) - downregulation and upregulation , cancer research , lung cancer , pi3k/akt/mtor pathway , cell growth , protein kinase b , medicine , cancer , cell , signal transduction , biology , microbiology and biotechnology , gene , biochemistry
Accumulating evidence has suggested that the dysregulation of mi RNA is an important factor in the pathogenesis of lung cancer. Here, we demonstrate that miR‐335 expression is reduced in non‐small cell lung cancer ( NSCLC ) tumors relative to non‐cancerous adjacent tissues, while the expression of Tra2β is increased. In addition, clinical data revealed that the increased Tra2β and decreased miR‐335 expression observed in NSCLC cells was associated with poor patient survival rates. In vitro experimentation showed that the overexpression of miR‐335 inhibited the growth, invasion and migration capabilities of A459 lung cancer cells, by targeting Tra2β. In contrast, inhibition of miR‐335 or overexpression of the Tra2β target gene stimulated the growth, invasion and migratory capabilities of A459 lung cancer cells in vitro. Furthermore, overexpression of miR‐335 or inhibition of Tra2β decreased the phosphorylation of Rb‐S780 and Rb‐ AKT . Overall, these findings suggest that the downregulation of miR‐335 in A459 lung cancer cells promoted cell proliferation through upregulation of Tra2β, mediated via activation of the AKT / mTOR signaling pathway, and suggest that miR‐335 may have potential as a novel therapeutic target for NSCLC .