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升高的S100A6（钙周期蛋白）增强透明细胞肾细胞癌的肿瘤发生并抑制CXCL14诱导的细胞凋亡。

Elevated S100A6 (Calcyclin) enhances tumorigenesis and suppresses CXCL14-induced apoptosis in clear cell renal cell carcinoma.

作者信息

Lyu Xiang-Jun, Li Hong-Zhao, Ma Xin, Li Xin-Tao, Gao Yu, Ni Dong, Shen Dong-Lai, Gu Liang-You, Wang Bao-Jun, Zhang Yu, Zhang Xu

机构信息

Department of Urology/State Key Laboratory of Kidney Diseases, Chinese People's Liberation Army General Hospital/PLA Medical School, Beijing, People's Republic of China.

Department of Urology, Zhongnan Hospital, Wuhan University, Wuhan, People's Republic of China.

出版信息

Oncotarget. 2015 Mar 30;6(9):6656-69. doi: 10.18632/oncotarget.3169.

DOI:10.18632/oncotarget.3169
PMID:25760073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4466641/
Abstract

Clear cell renal cell carcinoma (ccRCC) is often resistant to existing therapy. We found elevated S100A6 levels in ccRCC tissues, associated with higher grade pathological features and clinical stages in ccRCC patients. Knockdown of S100A6 inhibited cell proliferation in vitro and tumor growth in vivo. Gene expression profiling suggests a novel function of S100A6 in suppressing apoptosis, as well as a relationship between S100A6 and CXCL14, a pro-inflammatory chemokine. We suggest that the S100A6/CXCL14 signaling pathway is a potential therapeutic target in ccRCC.

摘要

透明细胞肾细胞癌（ccRCC）通常对现有治疗有抗性。我们发现ccRCC组织中S100A6水平升高，这与ccRCC患者更高分级的病理特征和临床分期相关。敲低S100A6可抑制体外细胞增殖和体内肿瘤生长。基因表达谱分析表明S100A6在抑制细胞凋亡方面具有新功能，以及S100A6与促炎趋化因子CXCL14之间存在关联。我们认为S100A6/CXCL14信号通路是ccRCC的一个潜在治疗靶点。

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