Insulin-like growth factor I activates the invasion suppressor function of E-cadherin in MCF-7 human mammary carcinoma cells in vitro - PubMed (original) (raw)

Insulin-like growth factor I activates the invasion suppressor function of E-cadherin in MCF-7 human mammary carcinoma cells in vitro

M E Bracke et al. Br J Cancer. 1993 Aug.

Free PMC article

Abstract

The calcium-dependent cell-cell adhesion molecule E-cadherin has been shown to counteract invasion of epithelial neoplastic cells. Using three monoclonal antibodies, we have demonstrated the presence of E-cadherin at the surface of human MCF-7/6 mammary carcinoma cells by indirect immunofluorescence coupled to flow cytometry and by immunocytochemistry. Nevertheless, MCF-7/6 cells failed to aggregate in a medium containing 1.25 mM CaCl2, and they were invasive after confrontation with embryonic chick heart fragments in organ culture. Treatment of MCF-7/6 cells with 0.5 microgram ml-1 insulin-like growth factor I (IGF-I) led to homotypic aggregation within 5 to 10 min and inhibited invasion in vitro during at least 8 days. The effect of IGF-I on cellular aggregation was insensitive to cycloheximide. However, monoclonal antibodies that interfered with the function of either the IGF-I receptor (alpha IR3) or E-cadherin (HECD-1, MB2) blocked the effect of IGF-I on aggregation. The effects of IGF-I on aggregation and on invasion could be mimicked by 1 microgram ml-1 insulin, but not by 0.5 microgram ml-1 IGF-II. The insulin effects were presumably not mediated by the IGF-I receptor, since they could not be blocked by an antibody against this receptor (alpha IR3). Our results indicate that IGF-I activates the invasion suppressor role of E-cadherin in MCF-7/6 cells.

PubMed Disclaimer

Cited by

Removal of sialic acid from the surface of human MCF-7 mammary cancer cells abolishes E-cadherin-dependent cell-cell adhesion in an aggregation assay.
Deman JJ, Van Larebeke NA, Bruyneel EA, Bracke ME, Vermeulen SJ, Vennekens KM, Mareel MM. Deman JJ, et al. In Vitro Cell Dev Biol Anim. 1995 Sep;31(8):633-9. doi: 10.1007/BF02634317. In Vitro Cell Dev Biol Anim. 1995. PMID: 8528519
The cadherin-catenin superfamily in endocrine tumors.
Semba S, Yamakawa M, Sasano H. Semba S, et al. Endocr Pathol. 2001 Spring;12(1):1-13. doi: 10.1385/ep:12:1:01. Endocr Pathol. 2001. PMID: 11478263 Review.
Protein kinase C activation upregulates intercellular adhesion of alpha-catenin-negative human colon cancer cell variants via induction of desmosomes.
van Hengel J, Gohon L, Bruyneel E, Vermeulen S, Cornelissen M, Mareel M, von Roy F. van Hengel J, et al. J Cell Biol. 1997 Jun 2;137(5):1103-16. doi: 10.1083/jcb.137.5.1103. J Cell Biol. 1997. PMID: 9166410 Free PMC article.
Sialylation of E-cadherin does not change the spontaneous or ET-18-OMe-mediated aggregation of MCF-7 human breast cancer cells.
Steelant WF, Recchi MA, Noë VT, Boilly-Marer Y, Bruyneel EA, Verbert A, Mareel MM, Delannoy P. Steelant WF, et al. Clin Exp Metastasis. 1999 May;17(3):245-53. doi: 10.1023/a:1006639804430. Clin Exp Metastasis. 1999. PMID: 10432010
The lipid phosphatase activity of PTEN is critical for stabilizing intercellular junctions and reverting invasiveness.
Kotelevets L, van Hengel J, Bruyneel E, Mareel M, van Roy F, Chastre E. Kotelevets L, et al. J Cell Biol. 2001 Dec 24;155(7):1129-35. doi: 10.1083/jcb.200105109. Epub 2001 Dec 24. J Cell Biol. 2001. PMID: 11756467 Free PMC article.

References

1. Biochem Biophys Res Commun. 1988 Apr 15;152(1):398-405 - PubMed
1. J Cell Sci. 1991 Mar;98 ( Pt 3):395-401 - PubMed
1. Cell. 1991 Jul 12;66(1):107-19 - PubMed
1. J Cell Biol. 1990 Jan;110(1):193-208 - PubMed
1. Nature. 1970 Aug 15;227(5259):680-5 - PubMed

Insulin-like growth factor I activates the invasion suppressor function of E-cadherin in MCF-7 human mammary carcinoma cells in vitro - PubMed (original) (raw)