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Estrogen up-regulates neuropeptide Y Y1 receptor expression in a human breast cancer cell line.
Cancer Res. 2006 Apr 01; 66(7):3706-14.CR

Abstract

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 3'5'-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 ERalpha. Similarly, estrogen increased Y1R mRNA expression in T-47D (ER+) but not in MDA-MB231 or MDA-MB468 (ER-) 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 ERalpha. 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.

Authors+Show Affiliations

Department of Internal Medicine, University of Cincinnati Medical Center, MSB 231 Albert Sabin Way, Cincinnati, OH 45267, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

16585197

Citation

Amlal, Hassane, et al. "Estrogen Up-regulates Neuropeptide Y Y1 Receptor Expression in a Human Breast Cancer Cell Line." Cancer Research, vol. 66, no. 7, 2006, pp. 3706-14.
Amlal H, Faroqui S, Balasubramaniam A, et al. Estrogen up-regulates neuropeptide Y Y1 receptor expression in a human breast cancer cell line. Cancer Res. 2006;66(7):3706-14.
Amlal, H., Faroqui, S., Balasubramaniam, A., & Sheriff, S. (2006). Estrogen up-regulates neuropeptide Y Y1 receptor expression in a human breast cancer cell line. Cancer Research, 66(7), 3706-14.
Amlal H, et al. Estrogen Up-regulates Neuropeptide Y Y1 Receptor Expression in a Human Breast Cancer Cell Line. Cancer Res. 2006 Apr 1;66(7):3706-14. PubMed PMID: 16585197.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Estrogen up-regulates neuropeptide Y Y1 receptor expression in a human breast cancer cell line. AU - Amlal,Hassane, AU - Faroqui,Somia, AU - Balasubramaniam,Ambikaipakan, AU - Sheriff,Sulaiman, PY - 2006/4/6/pubmed PY - 2006/5/23/medline PY - 2006/4/6/entrez SP - 3706 EP - 14 JF - Cancer research JO - Cancer Res. VL - 66 IS - 7 N2 - 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 3'5'-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 ERalpha. Similarly, estrogen increased Y1R mRNA expression in T-47D (ER+) but not in MDA-MB231 or MDA-MB468 (ER-) 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 ERalpha. 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. SN - 0008-5472 UR - https://www.unboundmedicine.com/medline/citation/16585197/Estrogen_up_regulates_neuropeptide_Y_Y1_receptor_expression_in_a_human_breast_cancer_cell_line_ L2 - http://cancerres.aacrjournals.org/cgi/pmidlookup?view=long&pmid=16585197 DB - PRIME DP - Unbound Medicine ER -