期刊
CANCER RESEARCH
卷 71, 期 6, 页码 2183-2192出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-10-3626
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类别
资金
- NIH [RO1GM079451, RO1GM065899]
- MD Anderson Cancer Center
EGF activates NF-kappa B, and constitutively activated NF-kappa B contributes to EGFR mutation-associated tumorigenesis, but it remains unclear precisely how EGFR signaling leads to NF-kappa B activation. Here we report that CARMA3, a caspase recruitment domain (CARD)-containing scaffold molecule, is required for EGF-induced NF-kappa B activation. CARMA3 deficiency impaired the activation of the IKK complex following EGF stimulation, resulting in a defect of EGF-induced I kappa B alpha phosphorylation and NF-kappa B activation. We found that CARMA3 and Bcl10 contributed to several characteristics of EGFR-associated malignancy, including proliferation, survival, migration, and invasion. Most importantly, CARMA3 contributed to tumor growth in vivo. Our findings elucidate a crucial link between EGFR-proximal signaling components and the downstream IKK complex, and they suggest a new therapeutic target for treatment of EGFR-driven cancers. Cancer Res; 71(6); 2183-92. (C) 2011 AACR.
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