Reference : Oncostatin M up-regulates the ER chaperone Grp78/BiP in liver cells

	Document type :	Scientific journals : Article
	Discipline(s) :	Life sciences : Biochemistry, biophysics & molecular biology
	To cite this reference:	http://hdl.handle.net/10993/16412

Title :	Oncostatin M up-regulates the ER chaperone Grp78/BiP in liver cells
Language :	English
Author, co-author :	Vollmer, Stefan [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit > Signal Transduction Laboratory]
	Haan, Claude [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit >]
	Behrmann, Iris [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Life Science Research Unit >]
Publication date :	2010
Journal title :	Biochemical Pharmacology
Publisher :	Elsevier Science
Volume :	80
Issue/season :	12
Pages :	2066-2073
Peer reviewed :	Yes (verified by ORBilu)
Audience :	International
ISSN :	0006-2952
City :	Oxford
Country :	United Kingdom
Keywords :	[en] Cytokine signal transduction; Cytokines; Grp78/BiP; Jak/STAT; MAP kinases; Oncostatin M
Abstract :	[en] OSM, a cytokine of the IL-6-type cytokine family, regulates inflammatory processes (like the acute phase response), tissue remodeling, angiogenesis, cell differentiation and proliferation. Inflammation is discussed to favor carcinogenesis and the inflammatory cytokine OSM was lately described to up-regulate HIF-1α, whose up-regulation is also observed in many cancers. In this study we demonstrate that OSM, and to a lesser degree IL-6, induces the expression of Grp78/BiP, an ER chaperone associated with tumor development and poor prognosis in cancer. In contrast, IFN-γ or TNF-α had no effect on Grp78 expression. The up-regulation seems to be specific to liver cells, as it occurs in hepatocytes and hepatoma cells but not in prostate, melanoma, breast or kidney cells. OSM does not lead to up-regulation of Grp94, enhanced XBP-1 mRNA splicing or phosphorylation of eIF2α, indicating that it is not associated to a general ER stress response. Analysis of the underlying mechanism showed that Grp78 is up-regulated by transcriptional processes which are to the greater part, though not completely, dependent on MEK/Erk activation. © 2010 Elsevier Inc.
Permalink :	http://hdl.handle.net/10993/16412
DOI :	10.1016/j.bcp.2010.07.015
Other URL :	http://www.scopus.com/inward/record.url?eid=2-s2.0-78049437095&partnerID=40&md5=e85aa2e8c87c866dda758ffc87fc8b39
Commentary :	cited By (since 1996)3 Scopus

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