FoxD3 deficiency promotes breast cancer progression by induction of epithelial-mesenchymal transition.

Biochem Biophys Res Commun

Key Laboratory of Breast Cancer Prevention and Treatment of the Ministry of Education, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China; Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China. Electronic address:

Published: April 2014

AI Article Synopsis

  • - FOXD3 is identified as a tumor suppressor that is crucial for regulating the development and aggression of breast cancer cells, but its specific role in breast tumorigenesis is not well understood.
  • - Research shows that FOXD3 levels are lower in breast cancer tissues, and patients with decreased FOXD3 expression tend to have worse outcomes; its depletion encourages cancer cell growth and invasion.
  • - Enhancing FOXD3 expression can reduce breast cancer cell proliferation and invasion, suggesting its potential as a therapeutic target for improving breast cancer treatments.

Article Abstract

The transcription factor forkhead box D3 (FOXD3) plays an important role in the development of neural crest and gastric cancer cells. However, the function and mechanisms of FOXD3 in the breast tumorigenesis and progression is still limited. Here, we report that FOXD3 is a tumor suppressor of breast cancer tumorigenicity and aggressiveness. We found that FOXD3 is down-regulated in breast cancer tissues. Patients with low FOXD3 expression have a poor outcome. Depletion of FOXD3 expression promotes breast cancer cell proliferation and invasion in vitro, whereas overexpression of FOXD3 inhibits breast cancer cell proliferation and invasion both in vitro and in vivo. In addition, depletion of FOXD3 is linked to epithelial-mesenchymal transition (EMT)-like phenotype. Our results indicate FOXD3 exhibits tumor suppressive activity and may be useful for breast therapy.

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http://dx.doi.org/10.1016/j.bbrc.2014.03.019DOI Listing

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