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NPY1R exerts inhibitory action on estradiol-stimulated growth and predicts endocrine sensitivity and better survival in ER-positive breast cancer
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NPY1R exerts inhibitory action on estradiol-stimulated growth and predicts endocrine sensitivity and better survival in ER-positive breast cancer
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Journal Article
NPY1R exerts inhibitory action on estradiol-stimulated growth and predicts endocrine sensitivity and better survival in ER-positive breast cancer
2022
Overview
G Protein-Coupled Receptors (GPCRs) represent the largest superfamily of cell-surface proteins. However, the expression and function of majority of GPCRs remain unexplored in breast cancer (BC). We interrogated the expression and phosphorylation status of 398 non-sensory GPCRs using the landmark BC proteogenomics and phosphoproteomic dataset from The Cancer Genome Atlas. Neuropeptide Y Receptor Y1 (NPY1R) gene and protein expression were significantly higher in Luminal A tumors versus other BC subtypes. The trend of NPY1R gene, protein, and phosphosite (NPY1R-S368s) expression was decreasing in the order of Luminal A, Luminal B, Basal, and human epidermal growth factor receptor 2 (HER2) subtypes.
NPY1R
gene expression increased in response to estrogen and reduced with endocrine therapy in estrogen receptor-positive (ER+) BC cells and xenograft models. Conversely, NPY1R expression decreased in ER+ BC cells resistant to endocrine therapies (estrogen deprivation, tamoxifen, and fulvestrant) in vitro and in vivo. NPY treatment reduced estradiol-stimulated cell growth, which was reversed by NPY1R antagonist (BIBP-3226) in ER+ BC cells. Higher NPY1R gene expression predicted better relapse-free survival and overall survival in ER+ BC. Our study demonstrates that NPY1R mediates the inhibitory action of NPY on estradiol-stimulated growth of ER+ BC cells, and its expression serves as a biomarker to predict endocrine sensitivity and survival in ER+ BC patients.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 631/67
/ 692/53
/ Animals
/ Antineoplastic Agents, Hormonal - pharmacology
/ Breast Neoplasms - drug therapy
/ Breast Neoplasms - pathology
/ Cell Proliferation - drug effects
/ Drug Resistance, Neoplasm - drug effects
/ Endocrine Gland Neoplasms - drug therapy
/ Endocrine Gland Neoplasms - genetics
/ Endocrine Gland Neoplasms - pathology
/ Estrogen Receptor alpha - genetics
/ Female
/ Gene Expression Regulation, Neoplastic
/ Genomes
/ Humanities and Social Sciences
/ Humans
/ Mice
/ Neoplasm Recurrence, Local - drug therapy
/ Neoplasm Recurrence, Local - genetics
/ Neoplasm Recurrence, Local - pathology
/ Proteins
/ Receptors, G-Protein-Coupled - genetics
/ Receptors, Neuropeptide Y - genetics
/ Science
/ Survival
/ Tumors
