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

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

Research output: Contribution to journalArticle

3 Scopus citations


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
Issue number1-3
StatePublished - Nov 27 2009



  • Cell cycle
  • Gastrin-releasing peptide receptor
  • p38

ASJC Scopus subject areas

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

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