Open AccessmiR‐30d is related to asbestos exposure and inhibits migration and invasion in NCI ‐H2452 cells
Author(s) -
Ju Li,
Wu Wei,
Yin Xianhong,
Xiao Yun,
Jia Zhenyu,
Lou Jianlin,
Yu Min,
Ying Shibo,
Chen Tianhui,
Jiang Zhaoqiang,
Li Wei,
Chen Junqiang,
Zhang Xing,
Zhu Lijin
Publication year - 2017
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12274
Subject(s) - vimentin , asbestos , mesothelioma , mesothelial cell , apoptosis , cancer research , cell , epithelial–mesenchymal transition , in vitro , cell migration , microbiology and biotechnology , cell growth , medicine , pathology , chemistry , downregulation and upregulation , biology , gene , immunohistochemistry , materials science , biochemistry , metallurgy
Pleural malignant mesothelioma ( MM ) is a highly aggressive tumor that is typically related to asbestos exposure and has a latency of 20–60 years. Several micro RNA contribute to MM initiation and progression, but the mechanisms are not clear. Here, we found that miR‐30d is downregulated in the pleural MM cell line NCI ‐H2452, in the plasma of asbestos‐exposed individuals, and in asbestos‐exposed mesothelial cells. Furthermore, we investigated the influence of the overexpression of miR‐30d in pleural MM cells. We demonstrated that miR‐30d overexpression could suppress pleural MM cell proliferation, migration, and invasion in vitro and could promote cell apoptosis but could not significantly influence cell cycle. The mRNA and protein expression of vimentin and TWIST 1 decreased, and the mRNA expression of CDH 1 increased in NCI ‐H2452 cells that overexpressed miR‐30d. We therefore conclude that miR‐30d is related to asbestos exposure and inhibits cell migration and invasion by regulating the epithelial–mesenchymal transition in NCI ‐H2452 cells.