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Up-regulation
of CC chemokine, CCL3L1, and receptors, CCR3, CCR5 in human
glioblastoma that promotes cell growth
Jun Kouno, Hisaki Nagai,
Takemitsu Nagahata, Masamitsu Onda, Humio Yamaguchi, Koji Adachi,
Hiroshi Takahashi, Akira Teramoto, Mitsuru Emi
Department of Molecular
Biology, Institute of Gerontology, Nippon Medical School, 1-396
Kosugi-cho, Nakahara-ku, Kawasak, 211-8533, Japan [J.K, H.N., T.N.,
M.O., M.U.*]. Department of Neurosurgery, Nippon Medical School,
Kosugi, Kawasaki, Tokyo, Japan [J.K., H.Y., K.A., H.T., A.T.].
*Corresponding Author (memi@nms.ac.jp)
Human CC ligand 3-like protein
1 (CCL3L1), a member of the CC chemokine family, that induces MCP1 and
RANTES, exhibits a variety of proinflammatory activities including
chemotaxis, and functional and proliferative activation of leukocytes,
lymphocytes and macrophages. Its signal is transmitted through
transmembrane receptors, CC chemokine receptors, CCR1, CCR3 and
CCR5.
To examine gene expression of chemokine, CCL3L1, and its receptors,
CCR1, CCR3 and CCR5, we analyzed tumor tissues from 21 patients with
several types of primary gliomas. CCL3L1, CCR3 and CCR5 gene exhibited
over-expression in 70% (7/10), 60% (6/10), and 60% (6/10) of
glioblastoma, in comparison with lower frequencies seen in lower-grade
gliomas.
Transfection of CCL3L1-expression vector to glioblastoma cell line
enhanced proliferation of the tumor cells.
These data suggest that increased expression of the CCL3L1, CCR3 and
CCR5 chemokine-receptors system is involved in brain tumorigenesis,
especially in the progression of glioblastoma.
Keywords: CC chemokine receptor (CCR) 1,
CCL3L1, CCR3, CCR5, glioma, MIP1A, mRNA expression
Copyright © 2004 Kluwer Academic Publishers.
All rights reserved
Source: http://ipsapp009.kluweronline.com/IPS/content/ext/x/J/5042/I/126/A/6/abstract.htm
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