Bombesin enhances TGF-β growth inhibitory effect through apoptosis induction in intestinal epithelial cells

Xianghua Liu, Junmei Zhao, Fazhi Li, Yan shi Guo, Mark R. Hellmich, Courtney M. Townsend, Yanna Cao, Tien C. Ko

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

Mammalian intestinal epithelium undergoes continuous cell turn over, with cell proliferation in the crypts and apoptosis in the villus. Both transforming growth factor (TGF)-β and gastrin-releasing peptide (GRP) are involved in the regulation of intestinal epithelial cells for division, differentiation, adhesion, migration and death. Previously, we have shown that TGF-β and bombesin (BBS) synergistically induce cyclooxygenase-2 (COX-2) expression and subsequent prostaglandin E2 (PGE2) production through p38MAPK in rat intestinal epithelial cell line stably transfected with GRP receptor (RIE/GRPR), suggesting the interaction between TGF-β signaling pathway and GRPR. The current study examined the biological responses of RIE/GRPR cells to TGF-β and BBS. Treatment with TGF-β1 (40 pM) and BBS (100 nM) together synergistically inhibited RIE/GRPR growth and induced apoptosis. Pretreatment with SB203580 (10 μM), a specific inhibitor of p38MAPK, partially blocked the synergistic effect of TGF-β and BBS on apoptosis. In conclusion, BBS enhanced TGF-β growth inhibitory effect through apoptosis induction, which is at least partially mediated by p38MAPK.

Original languageEnglish (US)
Pages (from-to)26-31
Number of pages6
JournalRegulatory Peptides
Volume158
Issue number1-3
DOIs
StatePublished - Nov 27 2009

Keywords

  • Cell cycle
  • Gastrin-releasing peptide receptor
  • p38

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Endocrinology
  • Clinical Biochemistry
  • Cellular and Molecular Neuroscience

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