Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2000;18(1):67-75.
doi: 10.1023/a:1026519016213.

CD44 and beta1 integrins mediate ovarian carcinoma cell migration toward extracellular matrix proteins

R C Casey  1 , A P Skubitz
Affiliations

CD44 and beta1 integrins mediate ovarian carcinoma cell migration toward extracellular matrix proteins

R C Casey et al. Clin Exp Metastasis. 2000.

Abstract

Epithelial cancer of the ovary spreads by implantation of tumor cells onto the mesothelial cells that line the peritoneal cavity. The aim of this study was to identify the cell-matrix interactions that mediate ovarian carcinoma cell migration toward components of the mesothelial cell-associated extracellular matrix. The human ovarian carcinoma cell lines NIH:OVCAR5 and SKOV3 were analyzed by flow cytometry for the expression of cell surface receptors. The ability of those receptors to mediate ovarian carcinoma cell migration toward fibronectin, type IV collagen, and laminin was determined. A monoclonal antibody against the beta1 integrin subunit abrogated the migration of both cell lines toward the extracellular matrix proteins. Blocking antibodies against alpha integrin subunits suggest that ovarian carcinoma cell migration toward fibronectin is primarily mediated by the alpha5beta1 integrin, type IV collagen by the alpha2beta1 integrin, and laminin by the alpha6beta1 integrin. These results suggest that ovarian carcinoma cell migration is regulated by multiple beta1 integrin-matrix interactions. Significant reduction of cell migration was observed with a monoclonal antibody against CD44 that blocks the hyaluronan-binding site of CD44, but not with an antibody that binds at an alternate site on CD44. Intact hyaluronan and/or hyaluronan oligomers also inhibited cell migration, suggesting that the CD44-hyaluronan interaction provides an integrin-independent mechanism of control for ovarian carcinoma cell migration. These results suggest that ovarian carcinoma cell migration is regulated by both integrin-dependent mechanisms, involving the interaction of beta1 integrins with extracellular matrix proteins, and an integrin-independent mechanism that involves the interaction of CD44 and hyaluronan.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Biochem Cell Biol. 1996;74(6):785-98 - PubMed
    1. Cancer Res. 1993 Aug 15;53(16):3830-8 - PubMed
    1. Cancer Res. 1997 Apr 1;57(7):1228-32 - PubMed
    1. J Cell Biol. 1993 Jul;122(2):431-42 - PubMed
    1. Glycoconj J. 1997 Aug;14(5):611-22 - PubMed

Publication types

MeSH terms

LinkOut - more resources