Bombesin induces angiogenesis and neuroblastoma growth

Jung Hee Kang; Titilope A. Ishola; Naira Baregamian; Joshua M. Mourot; Piotr G. Rychahou; B. Mark Evers; Dai H. Chung

doi:10.1016/j.canlet.2007.02.007

Bombesin induces angiogenesis and neuroblastoma growth

Jung Hee Kang, Titilope A. Ishola, Naira Baregamian, Joshua M. Mourot, Piotr G. Rychahou, B. Mark Evers, Dai H. Chung

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

59 Scopus citations

Abstract

Gastrin-releasing peptide (GRP), the mammalian equivalent of bombesin (BBS), is a trophic factor for highly vascular neuroblastomas; its mechanisms of action in vivo are unknown. We sought to determine the effects of BBS on the growth of neuroblastoma xenografts and on angiogenesis. BBS significantly increased the growth of SK-N-SH and BE(2)-C human neuroblastomas; tumors demonstrated increased expression of angiogenic markers, PECAM-1 and VEGF, as well as phosphorylated (p)-Akt levels. RC-3095, a BBS/GRP antagonist, attenuated BBS-stimulated tumor growth and angiogenesis in vivo. GRP or GRPR silencing significantly inhibited VEGF as well as p-Akt and p-mTOR expression in vitro. Our findings demonstrate that BBS stimulates neuroblastoma growth and the expression of angiogenic markers. Importantly, these findings suggest that novel therapeutic agents, targeting BBS-mediated angiogenesis, may be useful adjuncts in patients with advanced-stage neuroblastomas.

Original language	English
Pages (from-to)	273-281
Number of pages	9
Journal	Cancer Letters
Volume	253
Issue number	2
DOIs	https://doi.org/10.1016/j.canlet.2007.02.007
State	Published - Aug 18 2007

Bibliographical note

Funding Information:
The authors thank Karen Martin for manuscript preparation and Tatsuo Uchida for statistical analysis. This work was supported by Grants RO1 DK61470, RO1 DK48498, RO1 CA104748 and PO1 DK35608 from the National Institutes of Health and an Institutional Research Grant (IRG-110376) from the American Cancer Society.

Funding

The authors thank Karen Martin for manuscript preparation and Tatsuo Uchida for statistical analysis. This work was supported by Grants RO1 DK61470, RO1 DK48498, RO1 CA104748 and PO1 DK35608 from the National Institutes of Health and an Institutional Research Grant (IRG-110376) from the American Cancer Society.

Funders	Funder number
National Institutes of Health (NIH)	IRG-110376
American Cancer Society-Michigan Cancer Research Fund
National Institute of Diabetes and Digestive and Kidney Diseases	R01DK048498

Keywords

Angiogenesis
Bombesin
GRP
Neuroblastoma
VEGF

ASJC Scopus subject areas

Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.canlet.2007.02.007

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title = "Bombesin induces angiogenesis and neuroblastoma growth",

abstract = "Gastrin-releasing peptide (GRP), the mammalian equivalent of bombesin (BBS), is a trophic factor for highly vascular neuroblastomas; its mechanisms of action in vivo are unknown. We sought to determine the effects of BBS on the growth of neuroblastoma xenografts and on angiogenesis. BBS significantly increased the growth of SK-N-SH and BE(2)-C human neuroblastomas; tumors demonstrated increased expression of angiogenic markers, PECAM-1 and VEGF, as well as phosphorylated (p)-Akt levels. RC-3095, a BBS/GRP antagonist, attenuated BBS-stimulated tumor growth and angiogenesis in vivo. GRP or GRPR silencing significantly inhibited VEGF as well as p-Akt and p-mTOR expression in vitro. Our findings demonstrate that BBS stimulates neuroblastoma growth and the expression of angiogenic markers. Importantly, these findings suggest that novel therapeutic agents, targeting BBS-mediated angiogenesis, may be useful adjuncts in patients with advanced-stage neuroblastomas.",

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author = "Kang, \{Jung Hee\} and Ishola, \{Titilope A.\} and Naira Baregamian and Mourot, \{Joshua M.\} and Rychahou, \{Piotr G.\} and Evers, \{B. Mark\} and Chung, \{Dai H.\}",

note = "Funding Information: The authors thank Karen Martin for manuscript preparation and Tatsuo Uchida for statistical analysis. This work was supported by Grants RO1 DK61470, RO1 DK48498, RO1 CA104748 and PO1 DK35608 from the National Institutes of Health and an Institutional Research Grant (IRG-110376) from the American Cancer Society.",

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doi = "10.1016/j.canlet.2007.02.007",

language = "English",

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AU - Kang, Jung Hee

AU - Ishola, Titilope A.

AU - Baregamian, Naira

AU - Mourot, Joshua M.

AU - Rychahou, Piotr G.

AU - Evers, B. Mark

AU - Chung, Dai H.

N1 - Funding Information: The authors thank Karen Martin for manuscript preparation and Tatsuo Uchida for statistical analysis. This work was supported by Grants RO1 DK61470, RO1 DK48498, RO1 CA104748 and PO1 DK35608 from the National Institutes of Health and an Institutional Research Grant (IRG-110376) from the American Cancer Society.

PY - 2007/8/18

Y1 - 2007/8/18

N2 - Gastrin-releasing peptide (GRP), the mammalian equivalent of bombesin (BBS), is a trophic factor for highly vascular neuroblastomas; its mechanisms of action in vivo are unknown. We sought to determine the effects of BBS on the growth of neuroblastoma xenografts and on angiogenesis. BBS significantly increased the growth of SK-N-SH and BE(2)-C human neuroblastomas; tumors demonstrated increased expression of angiogenic markers, PECAM-1 and VEGF, as well as phosphorylated (p)-Akt levels. RC-3095, a BBS/GRP antagonist, attenuated BBS-stimulated tumor growth and angiogenesis in vivo. GRP or GRPR silencing significantly inhibited VEGF as well as p-Akt and p-mTOR expression in vitro. Our findings demonstrate that BBS stimulates neuroblastoma growth and the expression of angiogenic markers. Importantly, these findings suggest that novel therapeutic agents, targeting BBS-mediated angiogenesis, may be useful adjuncts in patients with advanced-stage neuroblastomas.

AB - Gastrin-releasing peptide (GRP), the mammalian equivalent of bombesin (BBS), is a trophic factor for highly vascular neuroblastomas; its mechanisms of action in vivo are unknown. We sought to determine the effects of BBS on the growth of neuroblastoma xenografts and on angiogenesis. BBS significantly increased the growth of SK-N-SH and BE(2)-C human neuroblastomas; tumors demonstrated increased expression of angiogenic markers, PECAM-1 and VEGF, as well as phosphorylated (p)-Akt levels. RC-3095, a BBS/GRP antagonist, attenuated BBS-stimulated tumor growth and angiogenesis in vivo. GRP or GRPR silencing significantly inhibited VEGF as well as p-Akt and p-mTOR expression in vitro. Our findings demonstrate that BBS stimulates neuroblastoma growth and the expression of angiogenic markers. Importantly, these findings suggest that novel therapeutic agents, targeting BBS-mediated angiogenesis, may be useful adjuncts in patients with advanced-stage neuroblastomas.

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KW - GRP

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KW - VEGF

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Bombesin induces angiogenesis and neuroblastoma growth

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

UN SDGs

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