FOXP3 Is an X-Linked Breast Cancer Suppressor Gene and an Important Repressor of the HER-2/ErbB2 Oncogene

Abstract

(Cell 129, 1275–1286; June 29, 2007) We, the editors of Cell, were contacted by the authors of this article regarding a duplication in Figure 7 that was not identified in the previous 2008 correction. Dr. Yang Liu, the corresponding author, has determined that the error was introduced during revision of the manuscript. In preparing the final figure, three images from the experiment showing that Foxp3 expression inhibits the growth of drug-resistant clones in breast cancer cell lines shown in Figure 7A—SKBR3 cells transfected with Otc cDNA, SKBR3 cells with vector, and MCF-7 cells with Foxp3—were mistakenly inserted into Figure 7D showing that ectopic expression of ErbB2 abrogated Foxp3-mediated repression. These images were incorrectly presented as TSA cells transfected with ErbB2 + pEF1 vector, ErbB2 + Foxp3, and pcDNA6 vector + Foxp3, respectively. The authors no longer have access to the original data, and consequently, a correction is not possible. Given the age of the paper and that the duplication does not compromise the conclusions of the paper, based on the information available to us at this time, we believe that no further action is warranted. FOXP3 Is an X-Linked Breast Cancer Suppressor Gene and an Important Repressor of the HER-2/ErbB2 OncogeneZuo et al.CellJune 29, 2007In BriefThe 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 (Foxp3sf/+) 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. Full-Text PDF Open Archive