miR-155 Regulates Glioma Cells Invasion and Chemosensitivity by p38 Isforms In Vitro

被引:57
|
作者
Liu, Qiang [1 ,2 ]
Zou, Ran [1 ]
Zhou, Rouxi [3 ]
Gong, Chaofan [3 ]
Wang, Zhifei [2 ]
Cai, Tao [2 ]
Tan, Chaochao [2 ]
Fang, Jiasheng [1 ]
机构
[1] Cent S Univ, Xiangya Hosp, Dept Neurosurg, Changsha 410008, Hunan, Peoples R China
[2] Cent S Univ, Xiangya Hosp 3, Dept Neurosurg, Changsha 410008, Hunan, Peoples R China
[3] Cent S Univ, Xiangya Med Sch, Changsha 410008, Hunan, Peoples R China
关键词
microRNA; MAPK; TEMOZOLOMIDE; REACTIVE OXYGEN SPECIES; CHEMOSENSITIVITY; GLIOBLASTOMA; BREAST-CANCER; EXPRESSION; APOPTOSIS; GROWTH; TUMORS; ACCUMULATION; MICRORNAS; PATHWAY; TARGETS; MIR-21;
D O I
10.1002/jcb.25073
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 MAPK or stress-activated protein kinase 4 (SAPK4)] and MAPK14 (also known as p38 MAPK). 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. (c) 2014 Wiley Periodicals, Inc.
引用
收藏
页码:1213 / 1221
页数:9
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