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Neuropeptide Y (NPY) in tumor growth and progression: Lessons learned from pediatric oncology.
Neuropeptides. 2016 Feb; 55:55-66.N

Abstract

Neuropeptide Y (NPY) is a sympathetic neurotransmitter with pleiotropic actions, many of which are highly relevant to tumor biology. Consequently, the peptide has been implicated as a factor regulating the growth of a variety of tumors. Among them, two pediatric malignancies with high endogenous NPY synthesis and release - neuroblastoma and Ewing sarcoma - became excellent models to investigate the role of NPY in tumor growth and progression. The stimulatory effect on tumor cell proliferation, survival, and migration, as well as angiogenesis in these tumors, is mediated by two NPY receptors, Y2R and Y5R, which are expressed in either a constitutive or inducible manner. Of particular importance are interactions of the NPY system with the tumor microenvironment, as hypoxic conditions commonly occurring in solid tumors strongly activate the NPY/Y2R/Y5R axis. This activation is triggered by hypoxia-induced up-regulation of Y2R/Y5R expression and stimulation of dipeptidyl peptidase IV (DPPIV), which converts NPY to a selective Y2R/Y5R agonist, NPY(3-36). While previous studies focused mainly on the effects of NPY on tumor growth and vascularization, they also provided insight into the potential role of the peptide in tumor progression into a metastatic and chemoresistant phenotype. This review summarizes our current knowledge of the role of NPY in neuroblastoma and Ewing sarcoma and its interactions with the tumor microenvironment in the context of findings in other malignancies, as well as discusses future directions and potential clinical implications of these discoveries.

Authors+Show Affiliations

Department of Nursing, School of Nursing and Health Studies, Georgetown University, Washington, DC 20057, USA; Department of Human Science, School of Nursing and Health Studies, Georgetown University, Washington, DC 20057, USA.Department of Biochemistry and Molecular & Cellular Biology, Georgetown University Medical Center, Washington, DC 20057, USA. Electronic address: jbk4@georgetown.edu.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

26549645

Citation

Tilan, Jason, and Joanna Kitlinska. "Neuropeptide Y (NPY) in Tumor Growth and Progression: Lessons Learned From Pediatric Oncology." Neuropeptides, vol. 55, 2016, pp. 55-66.
Tilan J, Kitlinska J. Neuropeptide Y (NPY) in tumor growth and progression: Lessons learned from pediatric oncology. Neuropeptides. 2016;55:55-66.
Tilan, J., & Kitlinska, J. (2016). Neuropeptide Y (NPY) in tumor growth and progression: Lessons learned from pediatric oncology. Neuropeptides, 55, 55-66. https://doi.org/10.1016/j.npep.2015.10.005
Tilan J, Kitlinska J. Neuropeptide Y (NPY) in Tumor Growth and Progression: Lessons Learned From Pediatric Oncology. Neuropeptides. 2016;55:55-66. PubMed PMID: 26549645.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuropeptide Y (NPY) in tumor growth and progression: Lessons learned from pediatric oncology. AU - Tilan,Jason, AU - Kitlinska,Joanna, Y1 - 2015/10/26/ PY - 2015/07/31/received PY - 2015/10/25/revised PY - 2015/10/25/accepted PY - 2015/11/10/entrez PY - 2015/11/10/pubmed PY - 2016/12/16/medline KW - Ewing sarcoma KW - Neuroblastoma KW - Neuropeptide Y (NPY) KW - Tumor biology SP - 55 EP - 66 JF - Neuropeptides JO - Neuropeptides VL - 55 N2 - Neuropeptide Y (NPY) is a sympathetic neurotransmitter with pleiotropic actions, many of which are highly relevant to tumor biology. Consequently, the peptide has been implicated as a factor regulating the growth of a variety of tumors. Among them, two pediatric malignancies with high endogenous NPY synthesis and release - neuroblastoma and Ewing sarcoma - became excellent models to investigate the role of NPY in tumor growth and progression. The stimulatory effect on tumor cell proliferation, survival, and migration, as well as angiogenesis in these tumors, is mediated by two NPY receptors, Y2R and Y5R, which are expressed in either a constitutive or inducible manner. Of particular importance are interactions of the NPY system with the tumor microenvironment, as hypoxic conditions commonly occurring in solid tumors strongly activate the NPY/Y2R/Y5R axis. This activation is triggered by hypoxia-induced up-regulation of Y2R/Y5R expression and stimulation of dipeptidyl peptidase IV (DPPIV), which converts NPY to a selective Y2R/Y5R agonist, NPY(3-36). While previous studies focused mainly on the effects of NPY on tumor growth and vascularization, they also provided insight into the potential role of the peptide in tumor progression into a metastatic and chemoresistant phenotype. This review summarizes our current knowledge of the role of NPY in neuroblastoma and Ewing sarcoma and its interactions with the tumor microenvironment in the context of findings in other malignancies, as well as discusses future directions and potential clinical implications of these discoveries. SN - 1532-2785 UR - https://www.unboundmedicine.com/medline/citation/26549645/Neuropeptide_Y__NPY__in_tumor_growth_and_progression:_Lessons_learned_from_pediatric_oncology_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0143-4179(15)00112-2 DB - PRIME DP - Unbound Medicine ER -