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Title: FoxD3 deficiency promotes breast cancer progression by induction of epithelial–mesenchymal transition

Abstract

Highlights: • FOXD3 is down-regulated in breast cancer tissues. • FOXD3 inhibits breast cancer cell proliferation and invasion. • FoxD3 deficiency induces epithelial–mesenchymal transition. - 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.

Authors:
 [1];  [2];  [3]; ;  [2];  [2]
  1. Department of General Surgery, The People’s Hospital of Wuqing, Tianjin (China)
  2. Key Laboratory of Breast Cancer Prevention and Treatment of the Ministry of Education, Tianjin Medical University Cancer Institute and Hospital, Tianjin (China)
  3. Department of Respiration, Affiliated Hospital of Medical College of Chinese People’s Armed Police Force, Tianjin (China)
Publication Date:
OSTI Identifier:
22416358
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 446; Journal Issue: 2; Other Information: Copyright (c) 2014 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ANIMAL TISSUES; CELL PROLIFERATION; CUMULATIVE RADIATION EFFECTS; IN VITRO; IN VIVO; MAMMARY GLANDS; NEOPLASMS; PATIENTS; PHENOTYPE; THERAPY; TRANSCRIPTION FACTORS

Citation Formats

Chu, Tian-Li, Zhao, Hong-Meng, Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, Tianjin, Li, Yue, Chen, Ao-Xiang, Sun, Xuan, Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, Tianjin, Ge, Jie, and Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, Tianjin. FoxD3 deficiency promotes breast cancer progression by induction of epithelial–mesenchymal transition. United States: N. p., 2014. Web. doi:10.1016/J.BBRC.2014.03.019.
Chu, Tian-Li, Zhao, Hong-Meng, Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, Tianjin, Li, Yue, Chen, Ao-Xiang, Sun, Xuan, Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, Tianjin, Ge, Jie, & Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, Tianjin. FoxD3 deficiency promotes breast cancer progression by induction of epithelial–mesenchymal transition. United States. https://doi.org/10.1016/J.BBRC.2014.03.019
Chu, Tian-Li, Zhao, Hong-Meng, Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, Tianjin, Li, Yue, Chen, Ao-Xiang, Sun, Xuan, Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, Tianjin, Ge, Jie, and Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, Tianjin. 2014. "FoxD3 deficiency promotes breast cancer progression by induction of epithelial–mesenchymal transition". United States. https://doi.org/10.1016/J.BBRC.2014.03.019.
@article{osti_22416358,
title = {FoxD3 deficiency promotes breast cancer progression by induction of epithelial–mesenchymal transition},
author = {Chu, Tian-Li and Zhao, Hong-Meng and Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, Tianjin and Li, Yue and Chen, Ao-Xiang and Sun, Xuan and Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, Tianjin and Ge, Jie and Breast Surgery, Tianjin Medical University Cancer Institute and Hospital, Tianjin},
abstractNote = {Highlights: • FOXD3 is down-regulated in breast cancer tissues. • FOXD3 inhibits breast cancer cell proliferation and invasion. • FoxD3 deficiency induces epithelial–mesenchymal transition. - 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.},
doi = {10.1016/J.BBRC.2014.03.019},
url = {https://www.osti.gov/biblio/22416358}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 2,
volume = 446,
place = {United States},
year = {Fri Apr 04 00:00:00 EDT 2014},
month = {Fri Apr 04 00:00:00 EDT 2014}
}