| Literature DB >> 19800578 |
Lizhong Wang1, Runhua Liu, Weiquan Li, Chong Chen, Hiroto Katoh, Guo-Yun Chen, Beth McNally, Lin Lin, Penghui Zhou, Tao Zuo, Kathleen A Cooney, Yang Liu, Pan Zheng.
Abstract
Despite clear epidemiological and genetic evidence for X-linked prostate cancer risk, all prostate cancer genes identified are autosomal. Here, we report somatic inactivating mutations and deletion of the X-linked FOXP3 gene residing at Xp11.23 in human prostate cancer. Lineage-specific ablation of FoxP3 in the mouse prostate epithelial cells leads to prostate hyperplasia and prostate intraepithelial neoplasia. In both normal and malignant prostate tissues, FOXP3 is both necessary and sufficient to transcriptionally repress cMYC, the most commonly overexpressed oncogene in prostate cancer as well as among the aggregates of other cancers. FOXP3 is an X-linked prostate tumor suppressor in the male. Because the male has only one X chromosome, our data represent a paradigm of "single genetic hit" inactivation-mediated carcinogenesis.Entities:
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Year: 2009 PMID: 19800578 PMCID: PMC2758294 DOI: 10.1016/j.ccr.2009.08.016
Source DB: PubMed Journal: Cancer Cell ISSN: 1535-6108 Impact factor: 31.743