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miR‐155 Regulates Glioma Cells Invasion and Chemosensitivity by p38 Isforms In Vitro
Author(s) -
Liu Qiang,
Zou Ran,
Zhou Rouxi,
Gong Chaofan,
Wang Zhifei,
Cai Tao,
Tan Chaochao,
Fang Jiasheng
Publication year - 2015
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.25073
Subject(s) - gene knockdown , p38 mitogen activated protein kinases , cancer research , glioma , temozolomide , biology , protein kinase a , mapk/erk pathway , apoptosis , kinase , microbiology and biotechnology , genetics
The critical role of microRNAs in cancer development has been extensively described. miRNAs are both specific markers and putative therapy targets. miR‐155 has been identified to be an oncomiRNA and is highly expressed in several solid cancers, including glioblastoma. In this study, we found that miR‐155 is a good potential therapy target. Knockdown of miR‐155 sensitizes glioma cells to the chemotherapy of temozolomide (TMZ) by targeting the p38 isoforms mitogen‐activated protein kinase 13 [MAPK13, also known as p38 MAPKδ or stress‐activated protein kinase 4 (SAPK4)] and MAPK14 (also known as p38 MAPKα). As tumor suppressor genes, MAPK13 and MAPK14 play important roles in lowering the accumulation of reactive oxygen species (ROS), inducing cell apoptosis, and slowing the progression of cancer. Knockdown of miR‐155 enhanced the anticancer effect of TMZ on glioma by targeting the MAPK13 and MAPK14‐mediated oxidative stress and apoptosis, but did not affect the secretion of MMP2 and MMP9. J. Cell. Biochem. 116: 1213–1221, 2015. © 2014 Wiley Periodicals, Inc.