VIP receptor antagonists and chemotherapeutic drugs inhibit the growth of breast cancer cells

T. W. Moody; J. Leyton; D. Chan; D. C. Brenneman; M. Fridkin; E. Gelber; A. Levy; I. Gozes

doi:10.1023/A:1017994722130

VIP receptor antagonists and chemotherapeutic drugs inhibit the growth of breast cancer cells

T. W. Moody^*, J. Leyton, D. Chan, D. C. Brenneman, M. Fridkin, E. Gelber, A. Levy, I. Gozes

^*Corresponding author for this work

Human Molecular Genetics Biochemistry

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

52 Scopus citations

Abstract

The effects of vasoactive intestinal peptide (VIP) antagonists on breast cancer cells were investigated. (N-stearyl, norleucine¹⁷)VIP hybrid ((SN)VIPhyb) inhibited specific ¹²⁵I-VIP binding to MCF7, SKBR3, T47D ZR75-1 and MDA-MB231 cells with high affinity (IC₅₀ values of 0.03-0.06 μM). (SN)VIPhyb,1 μM, inhibited the ability of 10 nM VIP to cause elevation of cAMP and to increase c-fos mRNA. Micromolar concentrations of (SN)VIPhyb inhibited the proliferation of MDA-MB231 or MCF7 cells using a MTT and clonogenic assay. Using a MTT assay, (SN)VIPhyb enhanced the ability of taxol and doxorubicin to inhibit breast cancer growth. Using nude mice bearing MDA-MB231 xenografts, VIPhyb potentiated the ability of taxol to inhibit proliferation. The results indicate that VIP receptor antagonists increase the ability of chemotherapeutic drugs to kill breast cancer cells.

Original language	English
Pages (from-to)	55-64
Number of pages	10
Journal	Breast Cancer Research and Treatment
Volume	68
Issue number	1
DOIs	https://doi.org/10.1023/A:1017994722130
State	Published - 2001

Keywords

Antagonist
Breast cancer
Doxorubicin
Proliferation
Taxol
VIP

UN SDGs

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

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10.1023/A:1017994722130

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title = "VIP receptor antagonists and chemotherapeutic drugs inhibit the growth of breast cancer cells",

abstract = "The effects of vasoactive intestinal peptide (VIP) antagonists on breast cancer cells were investigated. (N-stearyl, norleucine17)VIP hybrid ((SN)VIPhyb) inhibited specific 125I-VIP binding to MCF7, SKBR3, T47D ZR75-1 and MDA-MB231 cells with high affinity (IC50 values of 0.03-0.06 μM). (SN)VIPhyb,1 μM, inhibited the ability of 10 nM VIP to cause elevation of cAMP and to increase c-fos mRNA. Micromolar concentrations of (SN)VIPhyb inhibited the proliferation of MDA-MB231 or MCF7 cells using a MTT and clonogenic assay. Using a MTT assay, (SN)VIPhyb enhanced the ability of taxol and doxorubicin to inhibit breast cancer growth. Using nude mice bearing MDA-MB231 xenografts, VIPhyb potentiated the ability of taxol to inhibit proliferation. The results indicate that VIP receptor antagonists increase the ability of chemotherapeutic drugs to kill breast cancer cells.",

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author = "Moody, {T. W.} and J. Leyton and D. Chan and {C. Brenneman}, D. and M. Fridkin and E. Gelber and A. Levy and I. Gozes",

year = "2001",

doi = "10.1023/A:1017994722130",

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AU - Moody, T. W.

AU - Leyton, J.

AU - Chan, D.

AU - C. Brenneman, D.

AU - Fridkin, M.

AU - Gelber, E.

AU - Levy, A.

AU - Gozes, I.

PY - 2001

Y1 - 2001

N2 - The effects of vasoactive intestinal peptide (VIP) antagonists on breast cancer cells were investigated. (N-stearyl, norleucine17)VIP hybrid ((SN)VIPhyb) inhibited specific 125I-VIP binding to MCF7, SKBR3, T47D ZR75-1 and MDA-MB231 cells with high affinity (IC50 values of 0.03-0.06 μM). (SN)VIPhyb,1 μM, inhibited the ability of 10 nM VIP to cause elevation of cAMP and to increase c-fos mRNA. Micromolar concentrations of (SN)VIPhyb inhibited the proliferation of MDA-MB231 or MCF7 cells using a MTT and clonogenic assay. Using a MTT assay, (SN)VIPhyb enhanced the ability of taxol and doxorubicin to inhibit breast cancer growth. Using nude mice bearing MDA-MB231 xenografts, VIPhyb potentiated the ability of taxol to inhibit proliferation. The results indicate that VIP receptor antagonists increase the ability of chemotherapeutic drugs to kill breast cancer cells.

AB - The effects of vasoactive intestinal peptide (VIP) antagonists on breast cancer cells were investigated. (N-stearyl, norleucine17)VIP hybrid ((SN)VIPhyb) inhibited specific 125I-VIP binding to MCF7, SKBR3, T47D ZR75-1 and MDA-MB231 cells with high affinity (IC50 values of 0.03-0.06 μM). (SN)VIPhyb,1 μM, inhibited the ability of 10 nM VIP to cause elevation of cAMP and to increase c-fos mRNA. Micromolar concentrations of (SN)VIPhyb inhibited the proliferation of MDA-MB231 or MCF7 cells using a MTT and clonogenic assay. Using a MTT assay, (SN)VIPhyb enhanced the ability of taxol and doxorubicin to inhibit breast cancer growth. Using nude mice bearing MDA-MB231 xenografts, VIPhyb potentiated the ability of taxol to inhibit proliferation. The results indicate that VIP receptor antagonists increase the ability of chemotherapeutic drugs to kill breast cancer cells.

KW - Antagonist

KW - Breast cancer

KW - Doxorubicin

KW - Proliferation

KW - Taxol

KW - VIP

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JO - Breast Cancer Research and Treatment

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IS - 1

ER -

VIP receptor antagonists and chemotherapeutic drugs inhibit the growth of breast cancer cells

Abstract

Keywords

UN SDGs

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