Transcriptomics

Dataset Information

425

Transcription profiling by array of human MCF7 cells expressing FOXP3


ABSTRACT: As we clarified before, the FOXP3 gene is an X-linked tumor suppressor gene in mammary carcinoma in both human and mouse. We also clarified that the ERBB2 and SKP2 oncogenes were transcriptionally under control of the FOXP3 gene product in mammary epithelial cells. In order to further clarify the FOXP3 down stream target genes in human breast cancer cells, we planed to conduct a microarray analysis of FOXP3-induced gene expression profiling. MCF7, a human breast cancer cell line, with FOXP3-tet-off system was cultured with and without Doxycyclin for 2 days. In the MCF7 cell cultured without Dox, the FOXP3 transcript was significantly induced as compared to the MCF7 cultured with Dox. Total RNA from MCF7 with and wihtout Dox were extracted by Qiagen's RNeasy column and they were applied to Affymetrix Human U133 2.0 array according to the manufacture's protocol. We clarified as yet unknown FOXP3 target genes in human epithelial cells, e.g., the p21 gene, by this analysis.

REANALYSED by: E-MTAB-73

ORGANISM(S): Homo sapiens  

SUBMITTER: Hiroto Katoh  

PROVIDER: E-MTAB-73 | ArrayExpress | 2009-08-12

REPOSITORIES: ArrayExpress

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Publications

FOXP3 up-regulates p21 expression by site-specific inhibition of histone deacetylase 2/histone deacetylase 4 association to the locus.

Liu Runhua R   Wang Lizhong L   Chen Guoyun G   Katoh Hiroto H   Chen Chong C   Liu Yang Y   Zheng Pan P  

Cancer research 20090310 6


p21 loss has been implicated in conferring oncogenic activity to known tumor suppressor gene KLF4 and cancer drug tamoxifen. Regulators of p21, therefore, play critical roles in tumorigenesis. Here, we report that X-linked tumor suppressor FOXP3 is essential for p21 expression in normal epithelia and that lack of FOXP3 is associated with p21 down-regulation in breast cancer samples. A specific FOXP3 binding site in the intron 1 is essential for p21 induction by FOXP3. FOXP3 specifically inhibite  ...[more]

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