Overexpressed CacyBP/SIP leads to the suppression of growth in renal cell carcinoma
Overexpressed CacyBP/SIP leads to the suppression of growth in renal cell carcinoma
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过度表达 CacyBP/SIP 会抑制肾细胞癌的生长。
DOI：
10.1016/j.bbrc.2007.03.080
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发表时间：
2007-05-18
影响因子：
3.1
通讯作者：
Fan, Daiming
中科院分区：
文献类型：
--
作者：
Sun, Shiren;Ning, Xiaoxuan;Fan, Daiming
钙周期蛋白结合蛋白/Siah-1相互作用蛋白（Calcyclin-binding protein/Siah-1-interacting protein，CacyBP/SIP）是S100的靶蛋白，是一种新的泛素化复合物，可导致β-catenin降解，与胃癌的恶性表型相关。然而，CacyBP/SIP在肾细胞癌中的作用仍不清楚。在本研究中，我们分析了CacyBP/SIP蛋白在人肾癌细胞和临床组织样品中的表达。研究了CacyBP/SIP对肾癌细胞恶性表型的调控作用。结果表明，CacyBP/SIP在肾癌组织和细胞系中表达明显下调。CacyBP/SIP在A498细胞中的异位过表达抑制了该细胞的增殖，并显著延迟了细胞周期进程，这可能与其通过降低β-catenin蛋白表达下调Cyclin D1有关。CacyBP/SIP还抑制软琼脂集落形成及其在裸鼠体内的致瘤性。综上所述，我们的工作表明，CacyBP/SIP，作为一个新的下调基因在肾细胞癌，抑制肾癌细胞的增殖和肿瘤的发生。(c)2007年爱思唯尔公司All rights reserved.
Calcyclin-binding protein/Siah-1-interacting protein (CacyBP/SIP), a target protein of S100, has been identified as a component of a novel ubiquitinylation complex leading to beta-catenin degradation, which was found to be related to the malignant phenotypes of gastric cancer. However, the roles of CacyBP/SIP in renal cell carcinoma still remain unclear. In the present study, we had analyzed the expression of the CacyBP/SIP protein in human renal cancer cells and clinical tissue samples. The possible roles of CacyBP/SIP in regulating the malignant phenotype of renal cancer cells were also investigated. The results demonstrated that the expression of CacyBP/SIP was markedly down-regulated in renal cell carcinoma tissues and cell lines. Ectopic overexpression of CacyBP/SIP in A498 cells inhibited the proliferation of this cell and delayed cell cycle progression significantly, which might be related to the down-regulation of Cyclin D1 through reducing beta-catenin protein. CacyBP/SIP also suppressed colony formation in soft agar and its tumorigenicity in nude mice. Taken together, our work showed that CacyBP/SIP, as a novel down-regulated gene in renal cell carcinoma, suppressed proliferation and tumorigenesis of renal cancer cells. (c) 2007 Elsevier Inc. All rights reserved.