NDLI: Intermittent hypoxia confers pro-metastatic gene expression selectively through NF-κB in inflammatory breast cancer cells.

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Intermittent hypoxia confers pro-metastatic gene expression selectively through NF-κB in inflammatory breast cancer cells.

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Intermittent hypoxia confers pro-metastatic gene expression selectively through NF-κB in inflammatory breast cancer cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gutsche, Katrin Randi, Elisa B. Blank, Volker Fink, Daniel Wenger, Roland H. Leo, Cornelia Scholz, Carsten C.
Description	Country affiliation: Switzerland Author Affiliation: Gutsche K ( Institute of Physiology, University of Zurich, 8057 Zurich, Switzerland); Randi EB ( Institute of Physiology, University of Zurich, 8057 Zurich, Switzerland); Blank V ( Lady Davis Institute for Medical Research, Department of Medicine & Department of Physiology, McGill University, Montreal, Quebec, Canada H3T 1E2.); Fink D ( Department of Gynecology, University Hospital of Zurich, 8091 Zurich, Switzerland.); Wenger RH ( Institute of Physiology, University of Zurich, 8057 Zurich, Switzerland); Leo C ( Department Women and Children, Cantonal Hospital Baden, 5404 Baden, Switzerland. Electronic address: cornelia.leo@ksb.ch.); Scholz CC ( Institute of Physiology, University of Zurich, 8057 Zurich, Switzerland. Electronic address: carsten.scholz@uzh.ch.)
Abstract	Inflammatory breast cancer (IBC) is the most aggressive form of breast cancer. Treatment options are limited and the mechanisms underlying its aggressiveness are poorly understood. Intermittent hypoxia (IH) causes oxidative stress and is emerging as important regulator of tumor metastasis. Vessels in IBC tumors have been shown to be immature, which is a primary cause of IH. We therefore investigated the relevance of IH for the modulation of gene expression in IBC cells in order to assess IH as potential regulator of IBC aggressiveness. Gene array analysis of IBC cells following chronic IH (45-60 days) demonstrated increased expression of pro-metastatic genes of the extracellular matrix, such as tenascin-C (TNC; an essential factor of the metastatic niche) and matrix metalloproteinase 9 (MMP9), and of pro-inflammatory processes, such as cyclooxygenase-2 (COX-2). Investigating the oxidative stress-dependent regulation of TNC, we found a gradual sensitivity on mRNA and protein levels. Oxidative stress activated NF-E2-related factor 2 (Nrf2), c-Jun N-terminal kinase (JNK), c-Jun and nuclear factor κB (NF-κB), but TNC upregulation was only dependent on NF-κB activation. Pharmacological inhibition of inhibitor of NF-κB (IκB ) phosphorylation as well as overexpression of IκB prevented TNC, MMP9 and COX-2 induction, whereas the pro-inflammatory cytokine interleukin-1ß (IL-1ß) increased their expression levels. Analysis of the gene array data showed NF-κB binding sites for 64% of all upregulated genes, linking NF-κB with IH-dependent regulation of pro-metastatic gene expression in IBC cells. Our results provide a first link between intermittent hypoxia and pro-metastatic gene expression in IBC cells, revealing a putative novel mechanism for the high metastatic potential of IBC.
File Format	HTM / HTML
ISSN	08915849
Journal	Free Radical Biology and Medicine
Volume Number	101
e-ISSN	18734596
Language	English
Publisher	Elsevier
Publisher Date	2016-12-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Physiology (medical) Biochemistry

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