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Clinicopathological Analysis of miRNA Expression in Breast Cancer Tissues by Using miRNA In Situ Hybridization
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FOXP3 and FOXP3-regulated microRNAs suppress SATB1 in breast cancer cells

N McInnes1, T J Sadlon, C Y Brown

  • 1Women's and Children's Health Research Institute, Molecular Immunology Laboratory, Women's and Children's Hospital, 72 King William Road, North Adelaide, SA 5006, Australia.

Oncogene
|July 12, 2011
PubMed

Insights

The transcription factor FOXP3 suppresses breast cancer by regulating the oncogene SATB1 through a novel feed-forward loop involving miR-7 and miR-155. Restoring FOXP3 function may offer new breast cancer treatments.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • The transcription factor FOXP3 acts as a tumor suppressor in breast and prostate epithelia.
  • The precise mechanisms underlying FOXP3's tumor-suppressive role are not fully understood.

Purpose of the Study:

  • To elucidate the mechanism of action for FOXP3 in preventing breast epithelial transformation.
  • To identify key regulatory pathways controlled by FOXP3 in breast cancer.

Main Methods:

  • Investigated the regulatory relationship between FOXP3 and the oncogene SATB1.
  • Utilized techniques to demonstrate direct repression of SATB1 by FOXP3.
  • Identified microRNAs (miRs) induced by FOXP3 that target SATB1.

Main Results:

  • Identified a feed-forward regulatory loop where FOXP3 suppresses SATB1 expression.
  • Demonstrated that SATB1 is a direct transcriptional target of FOXP3.
  • Showed that FOXP3 induces miR-7 and miR-155, which further target SATB1's 3'-UTR.

Conclusions:

  • FOXP3-regulated miRs are integral to FOXP3's mechanism in preventing breast epithelial cancerous transformation.
  • Restoring FOXP3 function and its regulated miRs presents a potential therapeutic strategy for breast cancer.

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