NDLI: Inflammation, but not hypoxia, mediated HIF-1α activation depends on COX-2

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Inflammation, but not hypoxia, mediated HIF-1α activation depends on COX-2

Content Provider	Scilit
Author	O'Brien, David R. Stasinopoulos, Ioannis Bhujwalla, Zaver M.
Copyright Year	2009
Description	The COX pathway has been a target for pharmaceutical intervention in diseases with a high inflammatory component ranging from asthma and Alzheimer's to arthritis and cancer. A major transcriptional promoter of the malignant phenotype, HIF-1α, has been observed to be regulated by the COX-2 product PGE2. Here we show that HIF-1α protein significantly accumulated in human breast cancer MDA-MB-231 cells in response to the pro-inflammatory cytokine IL-1β, but not in COX-2-silenced MDA-MB-231 cells. In contrast HIF-1α expression could be detected in COX-2-silenced cells in response to the hypoxia-mimetic agent CoCl2 and hypoxia. Gene expression profiling in COX-2-containing and COX-2-silenced cells showed that the hypoxia-induced transcriptional response is largely unaffected by COX-2 silencing. These data suggest that the profound effects of COX-2 silencing on inhibiting invasion, tumor growth, and metastasis from MDA-MB-231 cells are dependent on the induction of IL-1β-dependent COX-2 and HIF-1α but are independent of hypoxia.
Related Links	https://www.tandfonline.com/doi/pdf/10.4161/cbt.8.1.7079?needAccess=true https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058789/pdf
Ending Page	35
Page Count	5
Starting Page	31
ISSN	15384047
e-ISSN	15558576
DOI	10.4161/cbt.8.1.7079
Journal	Cancer Biology & Therapy
Issue Number	1
Volume Number	8
Language	English
Publisher	Informa UK Limited
Publisher Date	2009-01-01
Access Restriction	Open
Subject Keyword	Biochemistry and Molecular Biology Breast Cancer Inflammation Cox-2 Cox-2-silencing Hypoxia Hif-1α
Content Type	Text
Resource Type	Article
Subject	Cancer Research Pharmacology Molecular Medicine Oncology

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