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CCL17‐CCR4 axis promotes metastasis via ERK/MMP13 pathway in bladder cancer
Author(s) -
Zhao Hongda,
Bo Qiyu,
Wang Weifen,
Wang Rui,
Li Yan,
Chen Shouzhen,
Xia Yangyang,
Wang Wenfu,
Wang Yong,
Zhu Kejia,
Liu Lei,
Cui Jianfeng,
Wang Shuai,
Liu Qinggang,
Wu Zonglong,
Guo Hu,
Shi Benkang
Publication year - 2019
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.27494
Subject(s) - ccr4 , ccl17 , cancer research , bladder cancer , gene knockdown , mapk/erk pathway , medicine , downregulation and upregulation , chemokine , ccl22 , chemokine receptor , cancer , oncology , signal transduction , receptor , chemistry , biology , microbiology and biotechnology , apoptosis , biochemistry , gene
As an important chemokine receptor, the role of CCR4 in the progression of bladder cancer (BC) remains unknown. In this study, we have shown that CCR4 expression was upregulated in bladder carcinoma tissues compared with adjacent nontumor tissues. Kaplan‐Meier survival analysis revealed that CCR4 expression was an independent prognostic risk factor in BC patients, and the addition of CCL17 induced CCR4 production and promoted migration and invasion of BC cells. In addition, CCR4 knockdown significantly attenuated the migratory and invasive capabilities of BC cells. Mechanistically, CCL17‐CCR4 axis is involved in ERK1/2 signaling and could mediate the migration and invasion of BC cells by regulating MMP13 activation. This study suggests that CCR4 might represent a promising prognostic biomarker and a potential therapeutic option for BC.