期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2004
卷号：101
期号：18
页码：7112-7117
DOI：10.1073/pnas.0402048101
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：The basis of constitutive activation of NF-{kappa}B, essential for survival and resistance to apoptosis in many tumors, is not well understood. We find that transforming growth factor {beta}2 (TGF{beta}2), predominantly in its latent form, is secreted by several different types of tumor cell lines that exhibit constitutively active NF-{kappa}B and that TGF{beta}2 potently stimulates the activation of NF-{kappa}B in reporter cells. Suppression of TGF{beta}2 expression by small interfering RNA kills prostate cancer PC3 cells, indicating that the TGF{beta}2-NF-{kappa}B pathway is important for their viability. These findings identify TGF{beta}2 as a potential target for therapeutic strategies to inhibit the growth of tumor cells that depend on constitutively active NF-{kappa}B, or to sensitize them to treatment with cytotoxic drugs.
关键词：prostate cancer ; small interfering RNA ; ELISA ; Smad
