Document Detail


Contact with fibrillar collagen inhibits melanoma cell proliferation by up-regulating p27KIP1.
MedLine Citation:
PMID:  10944199     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 G(1)/S checkpoint and maintain high levels of p27(KIP1) mRNA and protein. In contrast, on nonfibrillar (denatured) collagen, the cells enter the cell cycle, and p27(KIP1) is down-regulated. These growth regulatory effects involve contact between type I collagen and the collagen-binding integrin alpha(2)beta(1), 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.
Authors:
P Henriet; Z D Zhong; P C Brooks; K I Weinberg; Y A DeClerck
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  97     ISSN:  0027-8424     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  2000 Aug 
Date Detail:
Created Date:  2000-10-05     Completed Date:  2000-10-05     Revised Date:  2013-06-11    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  10026-31     Citation Subset:  IM    
Affiliation:
Division of Hematology-Oncology, Department of Pediatrics, Childrens Hospital Los Angeles, California 90027, USA.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis
Cell Cycle / physiology*
Cell Cycle Proteins*
Cell Division / drug effects,  physiology*
Collagen / pharmacology,  physiology*
Cyclin-Dependent Kinase Inhibitor p27
Cyclin-Dependent Kinases / antagonists & inhibitors
Extracellular Matrix Proteins / physiology
Gene Expression Regulation, Neoplastic*
Humans
Integrins / genetics,  physiology
Kinetics
Melanoma
Microtubule-Associated Proteins / genetics*
Tumor Cells, Cultured
Tumor Suppressor Proteins*
Grant Support
ID/Acronym/Agency:
R01 CA42919/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Cell Cycle Proteins; 0/Extracellular Matrix Proteins; 0/Integrins; 0/Microtubule-Associated Proteins; 0/Tumor Suppressor Proteins; 147604-94-2/Cyclin-Dependent Kinase Inhibitor p27; 9007-34-5/Collagen; EC 2.7.11.22/Cyclin-Dependent Kinases
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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