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Title: FOXD1 promotes breast cancer proliferation and chemotherapeutic drug resistance by targeting p27

Highlights: • FOXD1 is up-regulated in breast cancer tissues. • FOXD1 promotes breast cancer cell proliferation and chemoresistance by inducing G1 to S transition. • FOXD1 transcriptionally suppresses p27 expression. - Abstract: Forkhead transcription factors are essential for diverse processes in early embryonic development and organogenesis. As a member of the forkhead family, FOXD1 is required during kidney development and its inactivation results in failure of nephron progenitor cells. However, the role of FOXD1 in carcinogenesis and progression is still limited. Here, we reported that FOXD1 is a potential oncogene in breast cancer. We found that FOXD1 is up-regulated in breast cancer tissues. Depletion of FOXD1 expression decreases the ability of cell proliferation and chemoresistance in MDA-MB-231 cells, whereas overexpression of FOXD1 increases the ability of cell proliferation and chemoresistance in MCF-7 cells. Furthermore, we observed that FOXD1 induces G1 to S phase transition by targeting p27 expression. Our results suggest that FOXD1 may be a potential therapy target for patients with breast cancer.
Authors:
; ;  [1] ; ;  [2] ;  [1] ;  [1]
  1. Department of Anesthesiology, The First Affiliated Hospital of the General Hospital of CPLA, Beijing 100048 (China)
  2. Department of Anesthesiology, The General Hospital of CPLA, Beijing 100853 (China)
Publication Date:
OSTI Identifier:
22416877
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 456; Journal Issue: 1; Other Information: Copyright (c) 2014 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ANIMAL TISSUES; CARCINOGENESIS; CELL CYCLE; CELL PROLIFERATION; DRUGS; KIDNEYS; MAMMARY GLANDS; NEOPLASMS; ONCOGENES; ONTOGENESIS; PATIENTS; PHASE TRANSFORMATIONS; THERAPY; TRANSCRIPTION FACTORS