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Title: Novel reciprocal regulation of cAMP signaling and apoptosis by orphan G-protein-coupled receptor GPRC5A gene expression

Abstract

GPRC5A is a member of G-protein-coupled receptors, which was originally identified as an all-trans-retinoic acid-induced gene. Although recent studies reported that this gene was highly expressed in the cancer cell lines and that GPRC5A might positively regulate cell proliferation, its mechanism remains unknown. We investigated the upstream and downstream signaling of GPRC5A and its biological function, and found that cAMP signaling is the novel GPRC5A induction pathway. When GPRC5A gene was overexpressed, intracellular cAMP concentration was decreased, and Gs{alpha} gene expression was downregulated. On the other hand, RNA interference of GPRC5A increased mRNA levels of Gs{alpha} and intracellular cAMP, reduced cell number, and induced apoptosis. Conversely, cell number was increased by GPRC5A overexpression. We first report the novel negative feedback model of cAMP signaling through GPRC5A gene expression. This evidence explains one of the mechanisms of the GPRC5A-regulated cell growth in some cancer cell lines.

Authors:
 [1];  [1];  [1];  [1];  [1];  [1];  [1]
  1. Department of Molecular and Cellular Pharmacology, Pharmacogenomics and Pharmacoinformatics, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu Mei 514-8507 (Japan)
Publication Date:
OSTI Identifier:
20857904
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 351; Journal Issue: 1; Other Information: DOI: 10.1016/j.bbrc.2006.10.016; PII: S0006-291X(06)02250-9; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; AMP; APOPTOSIS; BIOLOGICAL FUNCTIONS; CELL PROLIFERATION; GENE REGULATION; GENES; GTP-ASES; NEOPLASMS; RECEPTORS; RETINOIC ACID; RNA

Citation Formats

Hirano, Minoru, Zang, Liqing, Oka, Takehiko, Ito, Yoshiyuki, Shimada, Yasuhito, Nishimura, Yuhei, and Tanaka, Toshio. Novel reciprocal regulation of cAMP signaling and apoptosis by orphan G-protein-coupled receptor GPRC5A gene expression. United States: N. p., 2006. Web. doi:10.1016/j.bbrc.2006.10.016.
Hirano, Minoru, Zang, Liqing, Oka, Takehiko, Ito, Yoshiyuki, Shimada, Yasuhito, Nishimura, Yuhei, & Tanaka, Toshio. Novel reciprocal regulation of cAMP signaling and apoptosis by orphan G-protein-coupled receptor GPRC5A gene expression. United States. https://doi.org/10.1016/j.bbrc.2006.10.016
Hirano, Minoru, Zang, Liqing, Oka, Takehiko, Ito, Yoshiyuki, Shimada, Yasuhito, Nishimura, Yuhei, and Tanaka, Toshio. 2006. "Novel reciprocal regulation of cAMP signaling and apoptosis by orphan G-protein-coupled receptor GPRC5A gene expression". United States. https://doi.org/10.1016/j.bbrc.2006.10.016.
@article{osti_20857904,
title = {Novel reciprocal regulation of cAMP signaling and apoptosis by orphan G-protein-coupled receptor GPRC5A gene expression},
author = {Hirano, Minoru and Zang, Liqing and Oka, Takehiko and Ito, Yoshiyuki and Shimada, Yasuhito and Nishimura, Yuhei and Tanaka, Toshio},
abstractNote = {GPRC5A is a member of G-protein-coupled receptors, which was originally identified as an all-trans-retinoic acid-induced gene. Although recent studies reported that this gene was highly expressed in the cancer cell lines and that GPRC5A might positively regulate cell proliferation, its mechanism remains unknown. We investigated the upstream and downstream signaling of GPRC5A and its biological function, and found that cAMP signaling is the novel GPRC5A induction pathway. When GPRC5A gene was overexpressed, intracellular cAMP concentration was decreased, and Gs{alpha} gene expression was downregulated. On the other hand, RNA interference of GPRC5A increased mRNA levels of Gs{alpha} and intracellular cAMP, reduced cell number, and induced apoptosis. Conversely, cell number was increased by GPRC5A overexpression. We first report the novel negative feedback model of cAMP signaling through GPRC5A gene expression. This evidence explains one of the mechanisms of the GPRC5A-regulated cell growth in some cancer cell lines.},
doi = {10.1016/j.bbrc.2006.10.016},
url = {https://www.osti.gov/biblio/20857904}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 1,
volume = 351,
place = {United States},
year = {Fri Dec 08 00:00:00 EST 2006},
month = {Fri Dec 08 00:00:00 EST 2006}
}