Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Oncostatin M (OSM) is a cytokine of the IL-6 family that modulates the growth of various cell types, at least in vitro. We have recently described that OSM inhibits growth and changes cell morphology of human glioma cell lines. Although leukemia inhibitory factor (LIF) receptor components are also expressed by these cells, the response to LIF was significantly weaker compared to OSM. We have therefore analyzed the signal transduction pathways induced by these cytokines. While OSM induces a number of strong tyrosine phosphorylations, including Janus tyrosine kinases (Jak) and the signal transducer and activator of transcription (Stat) proteins, LIF induces only minor tyrosine phosphorylation of Tyk2 and Stat3. Specific activation of the tyrosine phosphatase SHP-2 as well as the mitogen-activated kinase 2 (MAPK2) was found in glioma cells upon OSM treatment. MAPK2 turns out to be a crucial mediator of the OSM effect in glioma cells since inhibition of MAPK activity by the Mek1 inhibitor PD98059 blocks the OSM-induced inhibition of DNA synthesis by about 70%.

Original publication

DOI

10.1006/mcbr.1999.0117

Type

Journal article

Journal

Molecular cell biology research communications : MCBRC

Publication Date

05/1999

Volume

1

Pages

109 - 116

Addresses

Clinic of Neurology, Westf. Wilhelms-Universität Münster, Germany. halfter@uni-muenster.de

Keywords

Tumor Cells, Cultured, Humans, Glioma, Mitogen-Activated Protein Kinase 1, Growth Inhibitors, Peptides, Proteins, Milk Proteins, DNA-Binding Proteins, Trans-Activators, Receptors, Cytokine, Proto-Oncogene Proteins, Interleukin-6, Lymphokines, Blotting, Western, Precipitin Tests, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Cell Differentiation, STAT1 Transcription Factor, STAT3 Transcription Factor, STAT5 Transcription Factor, Protein-Tyrosine Kinases, Oncostatin M, Leukemia Inhibitory Factor, Janus Kinase 2, Janus Kinase 1, Leukemia Inhibitory Factor Receptor alpha Subunit, Receptors, OSM-LIF, TYK2 Kinase