| Literature DB >> 17570480 |
Tao Zuo1, Lizhong Wang, Carl Morrison, Xing Chang, Huiming Zhang, Weiquan Li, Yan Liu, Yin Wang, Xingluo Liu, Michael W Y Chan, Jin-Qing Liu, Richard Love, Chang-Gong Liu, Virginia Godfrey, Rulong Shen, Tim H-M Huang, Tianyu Yang, Bae Keun Park, Cun-Yu Wang, Pan Zheng, Yang Liu.
Abstract
The X-linked Foxp3 is a member of the forkhead/winged helix transcription factor family. Germline mutations cause lethal autoimmune diseases in males. Serendipitously, we observed that female mice heterozygous for the "scurfin" mutation of the Foxp3 gene (Foxp3(sf/+)) developed cancer at a high rate. The majority of the cancers were mammary carcinomas in which the wild-type Foxp3 allele was inactivated and HER-2/ErbB2 was overexpressed. Foxp3 bound and repressed the HER-2/ErbB2 promoter. Deletion, functionally significant somatic mutations, and downregulation of the FOXP3 gene were commonly found in human breast cancer samples and correlated significantly with HER-2/ErbB2 overexpression, regardless of the status of HER-2 amplification. Our data demonstrate that FOXP3 is an X-linked breast cancer suppressor gene and an important regulator of the HER-2/ErbB2 oncogene.Entities:
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Year: 2007 PMID： 17570480 PMCID： PMC1974845 DOI： 10.1016/j.cell.2007.04.034
Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 41.582