¹Center for Radiological Research, College of Physicians and Surgeons of Columbia University, VC 11-218, 630 West 168th Street, New York, NY 10032, USA

Correspondence: Dr TK Hei, E-mail: tkhl@columbia.edu

Received 1 November 2001; Revised 7 March 2002; Accepted 21 March 2002.

Abstract

Interaction between cell and extracellular matrix plays a crucial role in tumour invasion and metastasis. Using an immortalised human bronchial epithelial (BEP2D) cell model, the study here shows that expression of Betaig-h3 gene, which encodes a secreted adhesion molecule induced by transforming growth factor-, is markedly decreased in several independently generated, radiation-induced tumour cell lines (TL1–TL5) relative to parental BEP2D cells. Transfection of Betaig-h3 gene into tumour cells resulted in a significant reduction in tumour growth. While integrin receptor 51 was overexpressed in tumour cells, its expression was corrected to the level found in control BEP2D cells after Betaig-h3 transfection. These data suggest that Betaig-h3 gene is involved in tumour progression by regulating integrin receptor 51. The findings provide strong evidence that the Betaig-h3 gene has tumour suppressor function in human BEP2D cell model and suggest a potential target for interventional therapy.