Gastrin stabilises β-catenin protein in mouse colorectal cancer cells

D. H. Song, J. C. Kaufman, L. Borodyansky, C. Albanese, R. G. Pestell, M. Michael Wolfe

Research output: Contribution to journalArticlepeer-review

11 Citations (Scopus)


As gastrin may play a role in the pathophysiology of gastrointestinal (GI) malignancies, the elucidation of the mechanisms governing gastrin-induced proliferation has recently gained considerable interest. Several studies have reported that a large percentage of colorectal tumours overexpress or stabilise the β-catenin oncoprotein. We thus sought to determine whether gastrin might regulate β-catenin expression in colorectal tumour cells. Amidated gastrin-17 (G-17), one of the major circulating forms of gastrin, not only enhanced β-catenin protein expression, but also one of its target genes, cyclin D1. Furthermore, activation of β-catenin-dependent transcription by gastrin was confirmed by an increase in LEF-1 reporter activity, as well as enhanced cyclin D1 promoter activity. Finally, G-17 prolonged the τ1/2 of β-catenin protein, demonstrating that gastrin appears to exert its mitogenic effects on colorectal tumour cells, at least in part, by stabilising β-catenin.

Original languageEnglish
Pages (from-to)1581-1587
Number of pages7
JournalBritish Journal of Cancer
Issue number8
Publication statusPublished - 25 Apr 2005
Externally publishedYes


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