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Semin Cancer Biol. 2002 Jun;12(3):219-29.

Putative role of 67 kDa elastin-laminin receptor in tumor invasion.

Author information

1
Département de Médecine, Center de recherché sur le vieillissement, Service de Gériatrie, Institut Universitaire de Gériatrie de Sherbrooke, 1036 rue Belvedere sud, Sherbrooke, Que., Canada J1H 4C4. tfulop@ocourrier.usherb.ca

Abstract

Cellular regulatory mechanisms normally maintain a delicate balance between cell proliferation, quiescence and death. The imbalance between these functions resulting from molecular intracellular changes is a key factor in tumorigenesis. Tumor cells detaching from the primary tumor possess a propension for invasion and metastasis formation. These tumor cells can attach, migrate, proliferate and grow in host tissue. The surrounding extracellular matrix (ECM) modulates these functions. It is now widely accepted that cell-matrix interactions play an important role in these processes. Most investigators concentrated their attention on the role of integrins in the above processes. There are, however, only scant data on the role of elastin and its receptors in tumor invasion. Nevertheless, experimental evidence indicates that the 67 kDa elastin-laminin receptor (ELR) subunit plays an important role in tumor invasion by mediating essential tumor cell functions leading to metastases. In this review we will concentrate on the putative role of the 67 kDa ELR subunit in tumor invasion.

PMID:
12083852
DOI:
10.1016/S1044-579X(02)00025-1
[Indexed for MEDLINE]

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