期刊
CANCER CELL
卷 15, 期 4, 页码 283-293出版社
CELL PRESS
DOI: 10.1016/j.ccr.2009.02.015
关键词
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资金
- National Institutes of Health [R01 CA1 22976, R01 CA1 15815, R01 CA1 15674, P50 CA1 07399]
- Harry Lloyd Charitable Trust
- Board of Governors at City of Hope
- Topercer family
- Mr. John Goldsmith, the Seraph Foundation
- Janney Fund
NF-kappa B (ReIA) is constitutively active in many cancers, where it upregulates antiapoptotic and other oncogenic genes. While proinflammatory stimulus-induced NF-kappa B activation involves IKK-dependent nuclear translocation, mechanisms for maintaining constitutive NF-kappa B activity in tumors have not been elucidated. We show here that maintenance of NF-kappa B activity in tumors requires Stat3, which is also frequently constitutively activated in cancer. Stat3 prolongs NF-kappa B nuclear retention through acetyltransferase p300-mediated RelA acetylation, thereby interfering with NF-kappa B nuclear export. Stat3-mediated maintenance of NF-kappa B activity occurs in both cancer cells and tumor-associated hematopoietic cells. Both murine and human cancers display highly acetylated RelA, which is associated with Stat3 activity. This Stat3/NF-kappa B interaction is thus central to both the transformed and nontransformed elements in tumors.
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