NDLI: Contact with fibrillar collagen inhibits melanoma cell proliferation by up-regulating p27KIP1

Content Provider	PubMed Central
Author	Henriet, Patrick Zhong, Zhi-duan Brooks, Peter C. Weinberg, Kenneth I. Declerck, Yves A.
Copyright Year	2000
Abstract	It is known that the extracellular matrix regulates normal cell proliferation, and it is assumed that anchorage-independent malignant cells escape this regulatory function. Here we demonstrate that human M24met melanoma cells remain responsive to growth regulatory signals that result from contact with type I collagen and that the effect on proliferation depends on the physical structure of the collagen. On polymerized fibrillar collagen, M24met cells are growth arrested at the G1/S checkpoint and maintain high levels of p27KIP1 mRNA and protein. In contrast, on nonfibrillar (denatured) collagen, the cells enter the cell cycle, and p27KIP1 is down-regulated. These growth regulatory effects involve contact between type I collagen and the collagen-binding integrin α2β1, which appears restricted in the presence of fibrillar collagen. Thus melanoma cells remain sensitive to negative growth regulatory signals originating from fibrillar collagen, and the proteolytic degradation of fibrils is a mechanism allowing tumor cells to escape these restrictive signals.
Related Links	http://dx.doi.org/10.1073/pnas.170290997
Ending Page	10031
Page Count	6
Starting Page	10026
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	18
Volume Number	97
Language	English
Publisher	The National Academy of Sciences
Publisher Date	2000-08-29
Access Restriction	Open
Rights Holder	The National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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