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

Abstract

// Xiang-Jun Lyu 1, * , Hong-Zhao Li 1, * , Xin Ma 1 , Xin-Tao Li 1 , Yu Gao 1 , Dong Ni 2 , Dong-Lai Shen 1 , Liang-You Gu 1 , Bao-Jun Wang 1 , Yu Zhang 1 , Xu Zhang 1 1 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 2 Department of Urology, Zhongnan Hospital, Wuhan University, Wuhan, People's Republic of China * These authors have contributed equally to this work Correspondence to: Xu Zhang, e-mail: dr.xuzhang@hotmail.com Keywords: clear cell renal cell carcinoma, tumorigenesis, S100A6, CXCL14, apoptosis Received: December 11, 2014      Accepted: January 18, 2015      Published: February 03, 2015 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.