Breast cancer growth is inhibited by vasoactive intestinal peptide (VIP) hybrid, a synthetic VIP receptor antagonist

Hasan Zia; Toyoaki Hida; Sonia Jakowlew; Michael Birrer; Yehoshua Gozes; Jean C. Reubi; Mati Fridkin; Illana Gozes; Terry W. Moody

Breast cancer growth is inhibited by vasoactive intestinal peptide (VIP) hybrid, a synthetic VIP receptor antagonist

Hasan Zia, Toyoaki Hida, Sonia Jakowlew, Michael Birrer, Yehoshua Gozes, Jean C. Reubi, Mati Fridkin, Illana Gozes, Terry W. Moody^*

^*Corresponding author for this work

Human Molecular Genetics Biochemistry

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

99 Scopus citations

Abstract

Breast cancer vasoactive intestinal peptide (VIP) receptors were characterized. Using in vitro autoradiographic techniques, ¹²⁵I-labeled VIP bound with high affinity to breast biopsy sections. ¹²⁵I-labeled VIP bound specifically to five breast cancer cell lines examined using receptor- binding techniques. Specific ¹²⁵I-labeled VIP binding to MDA-MB-231 cells was inhibited with high affinity by VIP and pituitary adenylate cyclase- activating polypeptide (IC₅₀ = 2 nM) and with moderate affinity by the VIP hybrid (IC₅₀ = 0.5 μM). VIP elevated the cAMP in a dose-dependent manner, and VIP hybrid (10 μM) inhibited the increase in cAMP caused by VIP. Using Northern blot analysis, VIP (10 nM) stimulated c-fos and c-myc mRNA, and the increase caused by VIP was reversed by the VIP hybrid. The VIP hybrid inhibited breast cancer growth in vitro and in vivo using nude mice bearing breast cancer xenografts. These data suggest that the VIP hybrid is a breast cancer VIP receptor antagonist.

Original language	English
Pages (from-to)	3486-3489
Number of pages	4
Journal	Cancer Research
Volume	56
Issue number	15
State	Published - 1 Aug 1996

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@article{1dc24b11ee5048169b6647d02378284b,

title = "Breast cancer growth is inhibited by vasoactive intestinal peptide (VIP) hybrid, a synthetic VIP receptor antagonist",

abstract = "Breast cancer vasoactive intestinal peptide (VIP) receptors were characterized. Using in vitro autoradiographic techniques, 125I-labeled VIP bound with high affinity to breast biopsy sections. 125I-labeled VIP bound specifically to five breast cancer cell lines examined using receptor- binding techniques. Specific 125I-labeled VIP binding to MDA-MB-231 cells was inhibited with high affinity by VIP and pituitary adenylate cyclase- activating polypeptide (IC50 = 2 nM) and with moderate affinity by the VIP hybrid (IC50 = 0.5 μM). VIP elevated the cAMP in a dose-dependent manner, and VIP hybrid (10 μM) inhibited the increase in cAMP caused by VIP. Using Northern blot analysis, VIP (10 nM) stimulated c-fos and c-myc mRNA, and the increase caused by VIP was reversed by the VIP hybrid. The VIP hybrid inhibited breast cancer growth in vitro and in vivo using nude mice bearing breast cancer xenografts. These data suggest that the VIP hybrid is a breast cancer VIP receptor antagonist.",

author = "Hasan Zia and Toyoaki Hida and Sonia Jakowlew and Michael Birrer and Yehoshua Gozes and Reubi, {Jean C.} and Mati Fridkin and Illana Gozes and Moody, {Terry W.}",

year = "1996",

month = aug,

day = "1",

language = "אנגלית",

volume = "56",

pages = "3486--3489",

journal = "Cancer Research",

issn = "0008-5472",

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T1 - Breast cancer growth is inhibited by vasoactive intestinal peptide (VIP) hybrid, a synthetic VIP receptor antagonist

AU - Zia, Hasan

AU - Hida, Toyoaki

AU - Jakowlew, Sonia

AU - Birrer, Michael

AU - Gozes, Yehoshua

AU - Reubi, Jean C.

AU - Fridkin, Mati

AU - Gozes, Illana

AU - Moody, Terry W.

PY - 1996/8/1

Y1 - 1996/8/1

N2 - Breast cancer vasoactive intestinal peptide (VIP) receptors were characterized. Using in vitro autoradiographic techniques, 125I-labeled VIP bound with high affinity to breast biopsy sections. 125I-labeled VIP bound specifically to five breast cancer cell lines examined using receptor- binding techniques. Specific 125I-labeled VIP binding to MDA-MB-231 cells was inhibited with high affinity by VIP and pituitary adenylate cyclase- activating polypeptide (IC50 = 2 nM) and with moderate affinity by the VIP hybrid (IC50 = 0.5 μM). VIP elevated the cAMP in a dose-dependent manner, and VIP hybrid (10 μM) inhibited the increase in cAMP caused by VIP. Using Northern blot analysis, VIP (10 nM) stimulated c-fos and c-myc mRNA, and the increase caused by VIP was reversed by the VIP hybrid. The VIP hybrid inhibited breast cancer growth in vitro and in vivo using nude mice bearing breast cancer xenografts. These data suggest that the VIP hybrid is a breast cancer VIP receptor antagonist.

AB - Breast cancer vasoactive intestinal peptide (VIP) receptors were characterized. Using in vitro autoradiographic techniques, 125I-labeled VIP bound with high affinity to breast biopsy sections. 125I-labeled VIP bound specifically to five breast cancer cell lines examined using receptor- binding techniques. Specific 125I-labeled VIP binding to MDA-MB-231 cells was inhibited with high affinity by VIP and pituitary adenylate cyclase- activating polypeptide (IC50 = 2 nM) and with moderate affinity by the VIP hybrid (IC50 = 0.5 μM). VIP elevated the cAMP in a dose-dependent manner, and VIP hybrid (10 μM) inhibited the increase in cAMP caused by VIP. Using Northern blot analysis, VIP (10 nM) stimulated c-fos and c-myc mRNA, and the increase caused by VIP was reversed by the VIP hybrid. The VIP hybrid inhibited breast cancer growth in vitro and in vivo using nude mice bearing breast cancer xenografts. These data suggest that the VIP hybrid is a breast cancer VIP receptor antagonist.

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SN - 0008-5472

VL - 56

SP - 3486

EP - 3489

JO - Cancer Research

JF - Cancer Research

IS - 15

ER -

Breast cancer growth is inhibited by vasoactive intestinal peptide (VIP) hybrid, a synthetic VIP receptor antagonist

Abstract

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