SOCS, inflammation, and cancer.

JAK-STAT Pub Date : 2013-07-01 Epub Date: 2013-08-15 DOI:10.4161/jkst.24053
Kyoko Inagaki-Ohara, Taisuke Kondo, Minako Ito, Akihiko Yoshimura
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引用次数: 170

Abstract

Signal transduction pathways elicited by cytokines and hormones have been shown to regulate distinct stages of development. Suppressor of cytokine signaling (SOCS) proteins are negative feedback regulators of cytokine signaling mediated by the JAK-STAT signaling pathway. In particular, SOCS1 and SOCS3 are potent inhibitors of JAKs and can play pivotal roles in inflammation, as well as in the development and progression of cancers. Abnormal expression of SOCS1 and SOCS3 in cancer cells has been reported in human carcinoma associated with dysregulation of signals from cytokine receptors, Toll-like receptors (TLRs), and hormone receptors, resulting in malignancies. In this review, we focus on the role of SOCS1 and SOCS3 in cancer development. In addition, the potential of SOCS as a therapeutic target and diagnostic aid will be discussed.

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SOCS,炎症和癌症。
细胞因子和激素引发的信号转导通路已被证明调节不同的发育阶段。细胞因子信号传导抑制因子(SOCS)蛋白是由JAK-STAT信号通路介导的细胞因子信号的负反馈调节因子。特别是,SOCS1和SOCS3是JAKs的有效抑制剂,在炎症以及癌症的发生和进展中发挥关键作用。据报道,在人类癌症中,SOCS1和SOCS3在癌细胞中的异常表达与细胞因子受体、toll样受体(TLRs)和激素受体的信号失调有关,从而导致恶性肿瘤。本文就SOCS1和SOCS3在肿瘤发生中的作用进行综述。此外,还将讨论SOCS作为治疗靶点和诊断辅助手段的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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