Exogenous regucalcin suppresses the proliferation of human breast cancer MDA-MB-231 bone metastatic cells in vitro

• Type of Material: Article
• Authors: Masayoshi Yamaguchi, Emory University; Tomiyasu Murata, Meijo University
• Language: English
• Date: 2015-09-23
• Publisher: Spandidos Publications
• Publication Version: Final Published Version
• Copyright Statement: © Spandidos Publications 2015
• Final Published Version (URL): http://dx.doi.org/10.3892/mmr.2015.4352
• Title of Journal or Parent Work: Molecular Medicine Reports
• ISSN: 1791-2997
• Volume: 12
• Issue: 5
• Start Page: 7801
• End Page: 7805
• Keywords: carcinogenesis; regucalcin; cell proliferation; MDA-MB-231 cells; apoptosis; cell signaling; breast cancer

Abstract

Regucalcin serves a pivotal role as a suppressor protein in signal transduction in various types of cells and tissues. The regucalcin gene, which is localized on the X chromosome, consists of seven exons and six introns. Reductions in the gene expression of regucalcin have been suggested to serve a role in hepatocarcinogenesis in animal models and human patients, indicating a potential role as a suppressor protein in cancer. The aim of the current study was to investigate the effect of exogenous regucalcin on cell proliferation in the cloned human breast cancer MDA‑MB‑231 bone metastatic cell line in vitro. The proliferation of MDA‑MB‑231 cells was suppressed following the addition of regucalcin (0.1‑10 nM) in vitro. The suppression of proliferation was not enhanced in the presence of tumor necrosis factor‑α, PD98059, staurosporine, Bay K8644, wortmannin, 5,6‑dichloro‑1‑β‑D‑ribofuranosylbenzimidazole or gemcitabine. Exogenous regucalcin did not induce cell death in MDA‑MB‑231 cells in vitro. These data suggest that exogenous regucalcin possesses suppressive effects on the proliferation of human breast cancer MDA‑MB‑231 bone metastatic cells, and that this effect may be mediated through various intracellular signaling pathways in vitro. Exogenous regucalcin is suggested to function as a suppressor in cancer cell proliferation.