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ERK2依赖的CSN6磷酸化在结直肠癌发生过程中意义重大

ERK2-Dependent Phosphorylation of CSN6 Is Critical in Colorectal Cancer Development

来源:Scopus 发布时间:2015-9-15
作者:Fang L., Lu W., Choi H.H., Yeung S.C.J., Tung J.-Y., Hsiao C.-D., Fuentes-Mattei E., Menter D., Chen C., Wang L., Wang J., Lee M.-H.
机构: 中山大学附属第六医院 结直肠外科
期刊: CANCER CELL2015年2月2期28卷

Biomarkers for predicting prognosis are critical to treating colorectal cancer (CRC) patients. We found that CSN6, a subunit of COP9 signalosome, is overexpressed in CRC samples and that CSN6 overexpression is correlated with poor patient survival. Mechanistic studies revealed that CSN6 is deregulated by epidermal growth factor receptor (EGFR) signaling, in which ERK2 binds directly to CSN6 Leu163/Val165 and phosphorylates CSN6 at Ser148. Furthermore, CSN6 regulated β-Trcp and stabilized β-catenin expression by blocking the ubiquitin-proteasome pathway, thereby promoting CRC development. High CSN6 expression was positively correlated with ERK2 activation and β-catenin overexpression in CRC samples, and inhibiting CSN6 stability with cetuximab reduced colon cancer growth. Taken together, our study's findings indicate that the deregulation of β-catenin by ERK2-activated CSN6 is important for CRC development. Fang et al. show that CSN6, a subunit of the COP9 signalosome, is overexpressed in human colorectal cancer (CRC) samples and correlates with poor patient survival. Deregulated CSN6 by EGFR signaling stabilizes β-catenin via blocking the ubiquitin-proteasome pathway, thereby promoting CRC development. © 2015 Elsevier Inc..

 

通讯作者:Department of Colorectal Surgery, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou, China
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