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Blood, Vol. 92 No. 12 (December 15), 1998:
pp. 4700-4711
Functional Cooperation of Cyclin C and c-Myc in Mediating Homotypic
Cell Adhesion Via Very Late Antigen-4 Activation and Vascular Cell
Adhesion Molecule-1 Induction
Zhao-Jun Liu,
Yoshiya Tanaka,
Shinichiro Mine,
Akio Morinobu,
Hideo Yagita,
Ko Okumura,
Tadatsugu Taniguchi,
Hirohei Yamamura, and
Yasuhiro Minami
From the Department of Biochemistry and of Laboratory Medicine, Kobe
University, School of Medicine, Kobe, Japan; the First Department of
Internal Medicine, University of Occupational and Environmental Health,
School of Medicine, Kitakyushu, Japan; the Department of Immunology,
Juntendo University, School of Medicine, Tokyo, Japan; CREST (Core
Research for Evolutional Science and Technology) of Japan Science and
Technology Corporation (JST), Tokyo, Japan; and the Department of
Immunology, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
Very late antigen-4 (VLA-4)/vascular cell adhesion molecule-1
(VCAM-1) are a pair of adhesion molecules mediating cell-cell interaction. The binding activity of each depends on its surface expression, yet integrin activity can also be modulated through inside-out signaling. However, the specific intracellular molecules involved in modulating integrin VLA-4 activation via inside-out signaling or in regulating VCAM-1 expression are poorly understood. We
show here that constitutive coexpression of cyclin C and c-Myc in
hematopoietic BAF-B03 cells induces homotypic cell adhesion, which
results from enhanced VLA-4 ligand-binding activity and induced
expression of VCAM-1. Furthermore, regulation of cell adhesion appears
to be a feature unique to cyclin C, but not other G1 cyclins, E and D3,
and its regulatory function is independent of CDK8 kinase activity. Our
results provide a novel role for cyclin C and c-Myc in the regulation
of cell adhesion through distinct mechanisms.
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