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中国生物工程杂志

CHINA BIOTECHNOLOGY
中国生物工程杂志  2015, Vol. 35 Issue (9): 50-56    DOI: 10.13523/j.cb.20150908
综述     
SOCS3通过JNK和STAT3信号通路调控AKT
周立军, 刘文娟, 祁永浩, 李妙
天津大学药物科学与技术学院 天津 300072
SOCS3 Negatively Regulates AKT through JNK and STAT3 Signal Pathways
ZHOU Li-jun, LIU Wen-juan, QI Yong-hao, LI Miao
School of Pharmaceutical Science and Technology, Tianjin University, Tianjin 300072, China
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摘要:

蛋白激酶B(AKT),在细胞存活、代谢、迁移和侵袭等信号通路中起着重要的调控作用.细胞信号转导抑制因子3(SOCS3)主要参与酪氨酸蛋白激酶(JAK)/信号传导子和转录激活子3(STAT3)传导途径的负反馈调节,可能参与AKT的磷酸化,进而调控肿瘤的发生.根据SOCS3蛋白的生物学特性和AKT信号通路的激活途径,综述了SOCS3在AKT信号通路中的调控作用,以期针对SOCS3靶向AKT信号通路进行抗肿瘤研究,为肿瘤的治疗提供一种新的思路.

关键词: 细胞信号转导抑制因子3蛋白激酶B抗肿瘤磷酸化    
Abstract:

AKT, also known as protein kinase B, is a pivotal component of pathways associated with cell survival, metabolism, invasion and metastasis. Suppressor of cytokine signaling 3 (SOCS3) is a negative regulator of Janus protein kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) pathway and may involve in the phosphorylation of AKT and tumorigenesis. The review is focused on the biological function of SOCS3 and the role of SOCS3 in AKT signal pathway, which may be beneficial to targeting AKT signal pathway in cancer therapy.

Key words: SOCS3    AKT    Anti-tumor    Phosphorylation
收稿日期: 2015-05-18 出版日期: 2015-09-25
ZTFLH:  Q819  
通讯作者: 周立军     E-mail: lijunzhou@tju.edu.cn
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引用本文:

周立军, 刘文娟, 祁永浩, 李妙. SOCS3通过JNK和STAT3信号通路调控AKT[J]. 中国生物工程杂志, 2015, 35(9): 50-56.

ZHOU Li-jun, LIU Wen-juan, QI Yong-hao, LI Miao. SOCS3 Negatively Regulates AKT through JNK and STAT3 Signal Pathways. China Biotechnology, 2015, 35(9): 50-56.

链接本文:

https://manu60.magtech.com.cn/biotech/CN/10.13523/j.cb.20150908        https://manu60.magtech.com.cn/biotech/CN/Y2015/V35/I9/50


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