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Expression of short‐form oncostatin M receptor as a decoy receptor in lung adenocarcinomas
Author(s) -
Chen DR,
Chu CY,
Chen CY,
Yang HC,
Chiang YY,
Lin TY,
Chiang IP,
Chuang DY,
Yu CC,
Chow KC
Publication year - 2008
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.2361
Subject(s) - oncostatin m , decoy , leukemia inhibitory factor receptor , receptor , biology , cancer research , leukemia inhibitory factor , receptor expression , microbiology and biotechnology , cytokine , interleukin 6 , immunology , biochemistry
Oncostatin M (OSM) is a member of the interleukin‐6 (IL‐6) family of cytokines, and binds to the OSM receptor (OSMR) to inhibit cancer growth. Four forms of OSMR have been identified: leukemia inhibitory factor receptor (LIFR), OSMRβ, short‐form OSMR (OSMRs) and soluble OSMR (sOSMR). In this study, we examined the type and expression of OSMR in lung adenocarcinomas (LADCs). Expression of OSMR was determined by reverse transcription–polymerase chain reaction (RT–PCR), immunoblotting, immunohistochemistry and confocal immunofluorescent microscopy (CIM). Our results showed that, among the four forms of OSMR, OSMRs was mainly expressed in LADC, and expression level of OSMRs correlated with patient survival. CIM revealed that OSMRs was localized on the cell membrane of LADC cell lines in vitro . OSMRs acts as a decoy receptor by reducing the inhibitory effect of OSM on cell growth. Decrease in OSMRs expression by siRNA increased cell sensitivity to OSM, and ectopic expression of OSMRs reduced cell sensitivity to OSM. These results suggest that expression of OSMRs, which operates as a decoy receptor for OSM, is correlated with disease progression and adverse prognosis in patients with LADC. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.