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

doi:10.1016/j.regpep.2009.07.010

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

Surgery

Research output: Contribution to journal › Article › peer-review

5 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 p38^MAPK 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 p38^MAPK, 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 p38^MAPK.

Original language	English (US)
Pages (from-to)	26-31
Number of pages	6
Journal	Regulatory Peptides
Volume	158
Issue number	1-3
DOIs	https://doi.org/10.1016/j.regpep.2009.07.010
State	Published - 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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10.1016/j.regpep.2009.07.010

Cite this

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title = "Bombesin enhances TGF-β growth inhibitory effect through apoptosis induction in intestinal epithelial cells",

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.",

keywords = "Cell cycle, Gastrin-releasing peptide receptor, p38",

author = "Xianghua Liu and Junmei Zhao and Fazhi Li and Guo, \{Yan shi\} and Hellmich, \{Mark R.\} and Townsend, \{Courtney M.\} and Yanna Cao and Ko, \{Tien C.\}",

note = "Funding Information: We thank Dr. D. Song for technical support; M. Griffin in Flow Cytometry and Cell Sorting Core Facility, Univ. of Texas Medical Branch for flow cytometric analysis; E. Figueroa and S. Schuenke in the Department of Surgery, Univ. of Texas Medical Branch for manuscript preparation. This study was supported by Public Health Service grants P01 DK035608 (C.M.T. and T.C.K.) and R01 DK060105 (T.C.K.).",

year = "2009",

month = nov,

day = "27",

doi = "10.1016/j.regpep.2009.07.010",

language = "English (US)",

volume = "158",

pages = "26--31",

journal = "Regulatory Peptides",

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number = "1-3",

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T1 - Bombesin enhances TGF-β growth inhibitory effect through apoptosis induction in intestinal epithelial cells

AU - Liu, Xianghua

AU - Zhao, Junmei

AU - Li, Fazhi

AU - Guo, Yan shi

AU - Hellmich, Mark R.

AU - Townsend, Courtney M.

AU - Cao, Yanna

AU - Ko, Tien C.

N1 - Funding Information: We thank Dr. D. Song for technical support; M. Griffin in Flow Cytometry and Cell Sorting Core Facility, Univ. of Texas Medical Branch for flow cytometric analysis; E. Figueroa and S. Schuenke in the Department of Surgery, Univ. of Texas Medical Branch for manuscript preparation. This study was supported by Public Health Service grants P01 DK035608 (C.M.T. and T.C.K.) and R01 DK060105 (T.C.K.).

PY - 2009/11/27

Y1 - 2009/11/27

N2 - 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.

AB - 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.

KW - Cell cycle

KW - Gastrin-releasing peptide receptor

KW - p38

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UR - https://www.scopus.com/pages/publications/70349740790#tab=citedBy

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DO - 10.1016/j.regpep.2009.07.010

M3 - Article

C2 - 19631696

AN - SCOPUS:70349740790

SN - 0167-0115

VL - 158

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EP - 31

JO - Regulatory Peptides

JF - Regulatory Peptides

IS - 1-3

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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