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Neuropeptide Y Y5-receptor activation on breast cancer cells acts as a paracrine system that stimulates VEGF expression and secretion to promote angiogenesis.
Peptides. 2013 Oct; 48:106-13.P

Abstract

Accumulating data implicate a pathological role for sympathetic neurotransmitters like neuropeptide Y (NPY) in breast cancer progression. Our group and others reported that NPY promotes proliferation and migration in breast cancer cells, however the angiogenic potential of NPY in breast cancer is unknown. Herein we sought to determine if NPY promotes angiogenesis in vitro by increasing vascular endothelial growth factor (VEGF) expression and release from 4T1 breast cancer cells. Western blot analysis revealed that NPY treatment caused a 52 ± 14% increase in VEGF expression in the 4T1 cells compared to non-treated controls. Using selective NPY Y-receptor agonists (Y1R, Y2R and Y5R) we observed an increase in VEGF expression only when cells were treated with Y5R agonist. Congruently, using selective Y1R, Y2R, or Y5R antagonists, NPY-induced increases in VEGF expression in 4T1 cells were attenuated only under Y5R antagonism. Endothelial tube formation assays were conducted using conditioned media (CM) from NPY treated 4T1 cells. Concentration-dependent increases in number of branch points and complete endothelial networks were observed in HUVEC exposed to NPY CM. CM from Y5R agonist treated 4T1 cells caused similar increases in number of branch points and complete endothelial networks. VEGF concentration was quantified in CM (ELISA) from agonist experiments; we observed a 2-fold and 2.5-fold increase in VEGF release from NPY and Y5R agonist treated 4T1 cells respectively. Overall these data highlight a novel mechanism by which NPY may promote breast cancer progression, and further implicate a pathological role of the NPY Y5R.

Authors+Show Affiliations

Department of Medical Biophysics, Schulich School of Medicine & Dentistry, The University of Western Ontario, London, Ontario, Canada.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23932937

Citation

Medeiros, Philip J., and Dwayne N. Jackson. "Neuropeptide Y Y5-receptor Activation On Breast Cancer Cells Acts as a Paracrine System That Stimulates VEGF Expression and Secretion to Promote Angiogenesis." Peptides, vol. 48, 2013, pp. 106-13.
Medeiros PJ, Jackson DN. Neuropeptide Y Y5-receptor activation on breast cancer cells acts as a paracrine system that stimulates VEGF expression and secretion to promote angiogenesis. Peptides. 2013;48:106-13.
Medeiros, P. J., & Jackson, D. N. (2013). Neuropeptide Y Y5-receptor activation on breast cancer cells acts as a paracrine system that stimulates VEGF expression and secretion to promote angiogenesis. Peptides, 48, 106-13. https://doi.org/10.1016/j.peptides.2013.07.029
Medeiros PJ, Jackson DN. Neuropeptide Y Y5-receptor Activation On Breast Cancer Cells Acts as a Paracrine System That Stimulates VEGF Expression and Secretion to Promote Angiogenesis. Peptides. 2013;48:106-13. PubMed PMID: 23932937.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuropeptide Y Y5-receptor activation on breast cancer cells acts as a paracrine system that stimulates VEGF expression and secretion to promote angiogenesis. AU - Medeiros,Philip J, AU - Jackson,Dwayne N, Y1 - 2013/08/08/ PY - 2013/06/10/received PY - 2013/07/26/revised PY - 2013/07/26/accepted PY - 2013/8/13/entrez PY - 2013/8/13/pubmed PY - 2014/5/20/medline KW - 4T1, Mammary carcinoma KW - Ang1 KW - Ang2 KW - Breast cancer KW - CM KW - DMEM KW - Dulbecco's minimal essential medium KW - ELISA KW - FBS KW - FGF KW - Fetal bovine serum KW - HUVEC KW - IL-6 KW - MMP KW - NE KW - NPY KW - Neuropeptide Y KW - PDGF KW - TTBS KW - VEGF KW - Vascularization KW - Y1R KW - Y1agonist, KW - Y2R KW - Y2agoinst, KW - Y5R KW - Y5agonist KW - [Leu31, Pro34]-Neuropeptide Y KW - [cPP1-7, NPY19-23, Ala31, Aib32, Gln34]-hPancreatic polypeptide KW - angiopoietin 1 KW - angiopoietin 2 KW - conditioned media KW - enzyme-linked immunosorbent assay KW - fibroblast growth factor KW - human umbilical endothelial vein cells KW - interleukin 6 KW - matrix metalloproteinase KW - neuropeptide Y KW - norepinephrine KW - peptide YY (3–36) KW - platelet-derived growth factor KW - tris-buffered saline+Tween20 KW - vascular endothelial growth factor SP - 106 EP - 13 JF - Peptides JO - Peptides VL - 48 N2 - Accumulating data implicate a pathological role for sympathetic neurotransmitters like neuropeptide Y (NPY) in breast cancer progression. Our group and others reported that NPY promotes proliferation and migration in breast cancer cells, however the angiogenic potential of NPY in breast cancer is unknown. Herein we sought to determine if NPY promotes angiogenesis in vitro by increasing vascular endothelial growth factor (VEGF) expression and release from 4T1 breast cancer cells. Western blot analysis revealed that NPY treatment caused a 52 ± 14% increase in VEGF expression in the 4T1 cells compared to non-treated controls. Using selective NPY Y-receptor agonists (Y1R, Y2R and Y5R) we observed an increase in VEGF expression only when cells were treated with Y5R agonist. Congruently, using selective Y1R, Y2R, or Y5R antagonists, NPY-induced increases in VEGF expression in 4T1 cells were attenuated only under Y5R antagonism. Endothelial tube formation assays were conducted using conditioned media (CM) from NPY treated 4T1 cells. Concentration-dependent increases in number of branch points and complete endothelial networks were observed in HUVEC exposed to NPY CM. CM from Y5R agonist treated 4T1 cells caused similar increases in number of branch points and complete endothelial networks. VEGF concentration was quantified in CM (ELISA) from agonist experiments; we observed a 2-fold and 2.5-fold increase in VEGF release from NPY and Y5R agonist treated 4T1 cells respectively. Overall these data highlight a novel mechanism by which NPY may promote breast cancer progression, and further implicate a pathological role of the NPY Y5R. SN - 1873-5169 UR - https://www.unboundmedicine.com/medline/citation/23932937/Neuropeptide_Y_Y5_receptor_activation_on_breast_cancer_cells_acts_as_a_paracrine_system_that_stimulates_VEGF_expression_and_secretion_to_promote_angiogenesis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0196-9781(13)00269-6 DB - PRIME DP - Unbound Medicine ER -