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Author Yan, Jun-Hai ♦ Zhao, Chun-Liu ♦ Ding, Lan-Bao ♦ Zhou, Xi
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ ANGIOGENESIS ♦ ANIMAL TISSUES ♦ CARCINOGENESIS ♦ CELL CYCLE ♦ CELL PROLIFERATION ♦ GROWTH FACTORS ♦ IN VITRO ♦ IN VIVO ♦ LUNGS ♦ NEOPLASMS ♦ TRANSCRIPTION ♦ TRANSCRIPTION FACTORS
Abstract The transcription factor forkhead box D3 (FOXD3), widely studied as a transcriptional repressor in embryogenesis, participates in the carcinogenesis of many cancers. However, the expression pattern and role of FOXD3 in non-small cell lung cancer (NSCLC) have not been well characterized. We report that FOXD3 is significantly downregulated in NSCLC cell lines and clinical tissues. FOXD3 overexpression significantly inhibits cell growth and results in G1 cell cycle arrest in NSCLC A549 and H1299 cells. In a xenograft tumor model, FOXD3 overexpression inhibits tumor growth and angiogenesis. Remarkably, expression of vascular endothelial growth factor (VEGF) was reduced in FOXD3 overexpression models both in vitro and in vivo. These findings suggest that FOXD3 plays a potential tumor suppressor role in NSCLC progression and represents a promising clinical prognostic marker and therapeutic target for this disease. - Highlights: • FOXD3 is downregulated in NSCLC cell lines and tissues. • FOXD3 overexpression inhibited cell proliferation in NSCLC cells. • FOXD3 overexpression led to decreased angiogenesis in NSCLC cells in vitro and in vivo.
ISSN 0006291X
Educational Use Research
Learning Resource Type Article
Publisher Date 2015-10-09
Publisher Place United States
Journal Biochemical and Biophysical Research Communications
Volume Number 466
Issue Number 1


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