Interleukin-1β Affects MDAMB231 Breast Cancer Cell Migration under Hypoxia: Role of HIF-1α and NFκB Transcription Factors. (30th November 2015)

• Record Type: Journal Article
• Authors: Filippi, Irene; Carraro, Fabio; Naldini, Antonella
• Other Names: López-Collazo Eduardo Academic Editor.
• Is Part Of: Mediators of inflammation. Volume 2015(2015)
• Publication Date: 2015-11-30
• Subjects: Inflammation -- Mediators -- Periodicals; Biological response modifiers -- Periodicals; Inflammation (Pathologie) -- Médiateurs; Immunomodulateurs; Biological response modifiers; Inflammation -- Mediators; Immunology; Autacoids; Immunologic Factors; Cell Adhesion Molecules; Cell Communication; Cytokines; Inflammation; Periodicals; Electronic journals; 616.0473
• DOI: 10.1155/2015/789414
• Languages: English
• ISSNs: 0962-9351

Abstract

Abstract : Inflammation and tumor hypoxia are intimately linked and breast cancer provides a typical example of an inflammation-linked malignant disease. Indeed, breast cancer progression is actively supported by inflammatory components, including IL-1 β, and by the hypoxia-inducible factor- (HIF-) 1 α . In spite of many attempts where the role of either IL-1 β or HIF-1 α was evaluated, detailed mechanisms for their effects on breast cancer cell migration under hypoxia are still unclear. We here report that IL-1 β increased MDAMB231 cell migration under hypoxic conditions along with HIF-1 α accumulation and upregulation of CXCR1, which is transcriptionally regulated by HIF-1 α, as well as an increased expression of CXCL8 and NF κ B. In addition, IL-1 β -induced cell migration in hypoxia was not affected when HIF-1 α was inhibited by either siRNA or Topotecan, well known for its inhibitory effect on HIF-1 α . Of interest, HIF-1 α inhibition did not reduce NF κ B and CXCL8 expression and the reduction of IL-1 β -induced cell migration under hypoxia was achieved only by pharmacological inhibition of NF κ B. Our findings indicate that inhibition of HIF-1 α does not prevent the migratory program activated by IL-1 β in hypoxic MDAMB231 cells. They also suggest a potential compensatory role of NF κ B/CXCL8 pathway in IL-1 β -induced MDAMB231 cell migration in a hypoxic microenvironment.