Peptide YY Inhibits Growth of Human Breast Cancerin Vitroandin Vivo

Grisé, Kimberlee; Rongione, Anthony J.; Laird, Elizabeth C.; McFadden, David W.

doi:10.1006/jsre.1998.5528

Cited by 23 publications

(17 citation statements)

References 20 publications

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“…We have found that endogenous NPY stimulates apoptosis in SK-N-MC cells, whereas Y1/Y5R antagonists increase cell survival. Similar growth-inhibitory activities have been found for other NPY peptide family members, such as peptide YY, which inhibits proliferation of breast, prostate, and pancreatic cancer cells (44)(45)(46).…”

Section: Sk-n-be(2)supporting

confidence: 74%

Differential Effects of Neuropeptide Y on the Growth and Vascularization of Neural Crest–Derived Tumors

Kitlińska¹,

Abe²,

Kuo³

et al. 2005

Cancer Research

127

212

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Neuropeptide Y (NPY) is a sympathetic neurotransmitter recently found to be potently angiogenic and growth promoting for endothelial, vascular smooth muscle and neuronal cells. NPY and its cognate receptors, Y1, Y2 and Y5, are expressed in neural crest-derived tumors; however, their role in regulation of growth is unknown. The effect of NPY on the growth and vascularization of neuroendocrine tumors was tested using three types of cells: neuroblastoma, pheochromocytoma, and Ewing's sarcoma family of tumors (ESFT). The tumors varied in expression of NPY receptors, which was linked to differential functions of the peptide. NPY stimulated proliferation of neuroblastoma cells via Y2/Y5Rs and inhibited ESFT cell growth by Y1/Y5-mediated apoptosis. In both tumor types, NPY receptor antagonists altered basal growth levels, indicating a regulatory role of autocrine NPY. In addition, the peptide released from the tumor cells stimulated endothelial cell proliferation, which suggests its paracrine angiogenic effects. In nude mice xenografts, exogenous NPY stimulated growth of neuroblastoma tumors, whereas it increased apoptosis and reduced growth of ESFT. However, in both tumors, NPY treatment led to an increase in tumor vascularization. Taken together, this is the first report of NPY being a growth-regulatory factor for neuroendocrine tumors, acting both by autocrine activation of tumor cell proliferation or apoptosis and by angiogenesis. NPY and its receptors may become targets for novel approaches in the treatment of these diseases, directed against both tumor cell proliferation and angiogenesis. (Cancer Res 2005; 65(5): 1719-28)

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Section: Sk-n-be(2)supporting

confidence: 74%

Differential Effects of Neuropeptide Y on the Growth and Vascularization of Neural Crest–Derived Tumors

Kitlińska¹,

Abe²,

Kuo³

et al. 2005

Cancer Research

127

212

View full text Add to dashboard Cite

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“…The same inhibitory effects on cell proliferation after treatment with PYY were observed in breast cancer cells [27] and in some colon cancer cells (CaCo-2 and HCT-116) [40].…”

Section: Npy Peptide Family and Cell Prolife-rationsupporting

confidence: 69%

“…Moreover, PYY was found to significantly reduce the growth of human pancreatic ductal adenocarcinoma, both in vitro and in vivo models [25,26], and of human breast infiltrative ductal carcinoma [27]. PYY, first isolated in 1983 from porcine intestine [28], is a 36-aminoacid gut hormone predominantly secreted by the enterochromaffin cells of ileum, colon, and rectum in response to meal [29].…”

Section: Introductionmentioning

confidence: 99%

Relevance of the Neuropeptide Y System in the Biology of Cancer Progression

Ruscica¹,

Dozio²,

Motta³

et al. 2007

CTMC

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The peptides pancreatic polypeptide (PP), peptide YY (PYY), and neuropeptide Y (NPY) share a similar structure, known as PP-fold. Within this family of peptides, NPY, a highly conserved 36-aminoacid residue peptide, is involved in the regulation of a wide range of physiological functions, such as food intake and energy metabolism, as well as in the promotion of some remarkable aspects of tumor progression, including cell proliferation, matrix invasion, metastatization, and angiogenesis. NPY exerts its biological effects through five G-protein coupled receptors, named Y1-, Y2-, Y4-, Y5-, and y6-R, which appear associated with different aspects of oncogenesis. Y1-R seems involved in the modulation of cancer cell proliferation, whereas Y2-R activation appears to promote angiogenesis. The development of NPY receptor subtype selective analogs has helped to elucidate the physiological and pathophysiological role and localization of each receptor and may contribute to a better understanding of the receptor-ligand interaction. The NPY system appears to be variously associated with specific tumors, including neural crest-derived tumors, breast and prostate cancers. In addition to NPY, PYY is also able to affect cancer cell growth in a dose-dependent manner and through Y-Rs. In conclusion, peptides of the NPY family and the related receptors play an important role in the progression of different cancer types, with some molecular specificity according to each step of this process. On this basis, future studies may be directed to the implementation of novel diagnostic and therapeutic approaches targeting this system.

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“…However, our findings that estrogen up-regulates Y1R mRNA is of pathophysiologic importance in breast cancer. PYY-induced cAMP inhibition has been reported to be responsible for the inhibition of MCF-7 cell proliferation in vivo and in vitro (37). In contrast, overexpression of the regulatory subunits of protein kinase A in malignant breast tissue is associated with the induction of epithelial cell proliferation (38).…”

Section: Discussionmentioning

confidence: 99%

Estrogen Up-regulates Neuropeptide Y Y1 Receptor Expression in a Human Breast Cancer Cell Line

Amlal¹,

Faroqui²,

Balasubramaniam

et al. 2006

Cancer Research

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Normal breast tissue mainly expresses the neuropeptide Y (NPY) Y2 receptor whereas primary human breast carcinomas express the Y1 receptor (Y1R) subtype. We hypothesized that activation of estrogen signaling systems plays a role in the induction of Y1R. To investigate this possibility, we used estrogen receptor-positive (ER+) human breast carcinoma cell line, MCF-7, and examined the effect of estrogen on Y1R gene expression and its signaling pathways. Saturation binding studies revealed that MCF-7 cells express high-affinity NPY receptor. NPY inhibited forskolin-stimulated adenosine 3V 5V -cyclic monophosphate (cAMP) accumulation and mobilized intracellular Ca 2+ in MCF-7 cells. Chronic estrogen treatment enhanced NPY-mediated inhibition of cAMP accumulation by 4-fold and caused a significant increase in Y1R mRNA expression through ERA. Similarly, estrogen increased Y1R mRNA expression in T-47D (ER+) but not in MDA-MB231 or MDA-MB468 (ERÀ) cell lines. Cycloheximide decreased basal Y1R mRNA expression; however, it did not affect its increase by estrogen. Moreover, estrogen treatment of MCF-7 cells did not increase Y1R mRNA stability. The up-regulation of Y1R expression by estrogen is prevented by hydroxyurea but not by nocodazole or IB-MECA (cell cycle inhibitors). Lastly, NPY inhibited estrogen-induced cell proliferation through Y1R. In conclusion, MCF-7 cells express a functional Y1R coupled to both Ca 2+ and cAMP pathways. Estrogen up-regulates Y1R expression through ERA. This effect is independent of increased Y1R mRNA stability or new protein synthesis, and likely occurs during S phase completion of the cell cycle. Estrogen plays an important role in the up-regulation of Y1R, which in turn regulates estrogen-induced cell proliferation in breast cancer cells. (Cancer Res 2006; 66(7): 3706-14)

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Peptide YY Inhibits Growth of Human Breast Cancerin Vitroandin Vivo

Cited by 23 publications

References 20 publications

Differential Effects of Neuropeptide Y on the Growth and Vascularization of Neural Crest–Derived Tumors

Differential Effects of Neuropeptide Y on the Growth and Vascularization of Neural Crest–Derived Tumors

Relevance of the Neuropeptide Y System in the Biology of Cancer Progression

Estrogen Up-regulates Neuropeptide Y Y1 Receptor Expression in a Human Breast Cancer Cell Line

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