加拿大蒙特利尔大学和舍布鲁克大学的科学家发现了一种全新的预防癌症的分子机制。该研究详细解释了SOCS1分子是如何防止慢性炎症性疾病患者的大量致癌细胞因子的分子机制，发表在12月11日的Molecular Cell的杂志上。
据研究人员Dr. Gerardo Ferbeyre介绍，机体内细胞因子过多将增加癌症的发生。这项研究发现将有助于科学家针对那些患慢性炎症性疾病的病人开发出预防癌症的新方法，并有助于科学家更好地了解人类机体对抗癌症的天然防线。
课题组发现，SOCS1是p53基因的直接调节因子，当缺失SOCS1时，p53通路也会受到严重的影响，而人类许多癌症的发生就是因为p53基因丢失引起的。
这项新的研究表明，患者SOCS1缺失或许也会导致p53肿瘤抑制通路受阻；而将SOCS1分子导入到肿瘤细胞中，将会使肿瘤细胞处于永久休眠状态中，从而抑制癌细胞的无限增殖。（生物谷Bioon.com）
p53相关：
Nature Reviews Cancer：抑癌基因p53控制细胞基因开关机制
NSMB：抑癌基因p53活性调控机制
JBC：发现p53致癌机制
Cancer Cell综述：miRNA与p53的关系
AJHG：东亚人群p53基因多态性的适应机制
P53信号通路图
p53价格/报价搜索结果-抗体库-生物在线Lab-on-Web
生物谷推荐原始出处：
Molecular Cell, Volume 36, Issue 5, 754-767, 11 December 2009 doi:10.1016/j.molcel.2009.09.044
SOCS1 Links Cytokine Signaling to p53 and Senescence
Viviane Calabrese1, 3, Frédérick A. Mallette1, 3, 4, Xavier Deschênes-Simard1, Sheela Ramanathan2, Julien Gagnon2, Adrian Moores1, Subburaj Ilangumaran2, , and Gerardo Ferbeyre1, ,
1 Département de Biochimie, Université de Montréal, Montréal, Québec H3C 3J7, Canada
2 Immunology Division, Department of Pediatrics, Faculty of Medicine, University of Sherbrooke, Sherbrooke, Québec J1K 2R1, Canada
SOCS1 is lost in many human tumors, but its tumor suppression activities are not well understood. We report that SOCS1 is required for transcriptional activity, DNA binding, and serine 15 phosphorylation of p53 in the context of STAT5 signaling. In agreement, inactivation of SOCS1 disabled p53-dependent senescence in response to oncogenic STAT5A and radiation-induced apoptosis in T cells. In addition, SOCS1 was sufficient to induce p53-dependent senescence in fibroblasts. The mechanism of activation of p53 by SOCS1 involved a direct interaction between the SH2 domain of SOCS1 and the N-terminal transactivation domain of p53, while the C-terminal domain of SOCS1 containing the SOCS Box mediated interaction with the DNA damage-regulated kinases ATM/ATR. Also, SOCS1 colocalized with ATM at DNA damage foci induced by oncogenic STAT5A. Collectively, these results add another component to the p53 and DNA damage networks and reveal a mechanism by which SOCS1 functions as a tumor suppressor.
