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Overexpression of CXCL16 and its receptor CXCR6/Bonzo promotes growth of human schwannomas
Author(s) -
HeldFeindt Janka,
Rehmke Brigitte,
Mentlein Rolf,
Hattermann Kirsten,
Knerlich Friederike,
Hugo HeinzHermann,
Ludwig Andreas,
Mehdorn H. Maximilian
Publication year - 2008
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20651
Subject(s) - cxcl16 , biology , cancer research , mapk/erk pathway , chemokine , immunostaining , microbiology and biotechnology , signal transduction , schwannoma , receptor , chemokine receptor , immunology , pathology , immunohistochemistry , medicine , biochemistry
Abstract Chemokines and their receptors play a decisive role in tumor progression and metastasis. Here, we describe the expression of the CXCL16‐CXCR6‐system in human schwannomas of different localization and in malignant peripheral nerve sheath tumors. The transmembrane chemokine CXCL16 and its receptor CXCR6/Bonzo were overexpressed on the mRNA and protein levels in all tumor samples investigated as compared with normal peripheral or 8th cranial nerve tissues. Chromogenic immunostaining and confocal laser microscopy revealed that CXCL16 and CXCR6 were localized mainly on S‐100 positive schwannoma cells. Cultured schwannoma cells responded to CXCL16‐stimulation by phosphorylation of kinases p42/44 (Erk 2/1) that could be inhibited by the MEK1/2‐inhibitor U0126 indicating an involvement of the mitogen‐activated protein kinase signal transduction pathway. As a biological response, CXCL16 increased proliferation and induced migration of schwannomas. Hence, CXCL16 appears to be a novel growth factor for schwannomas of different localization. © 2008 Wiley‐Liss, Inc.