NDLI: Cobalt Chloride Induces Expression and Function of Breast Cancer Resistance Protein (BCRP/ABCG2) in Human Renal Proximal Tubular Epithelial Cell Line HK-2.

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Cobalt Chloride Induces Expression and Function of Breast Cancer Resistance Protein (BCRP/ABCG2) in Human Renal Proximal Tubular Epithelial Cell Line HK-2.

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Cobalt Chloride Induces Expression and Function of Breast Cancer Resistance Protein (BCRP/ABCG2) in Human Renal Proximal Tubular Epithelial Cell Line HK-2.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Nishihashi, Katsuki Kawashima, Kei Nomura, Takami Urakami-Takebayashi, Yumiko Miyazaki, Makoto Takano, Mikihisa Nagai, Junya
Description	Author Affiliation: Nishihashi K ( Laboratory of Pharmaceutics, Osaka University of Pharmaceutical Sciences.)
Abstract	The human breast cancer resistance protein (BCRP/ABCG2), a member of the ATP-binding cassette transporter family, is a drug transporter restricting absorption and enhancing excretion of many compounds including anticancer drugs. The cis-regulatory elements in the BCRP promoter include a hypoxia response element, i.e., the DNA binding site for hypoxia-inducible factor-1 (HIF-1). In this study, we investigated the effect of cobalt chloride, a chemical inducer of HIF-1 , on the expression and function of BCRP in human renal proximal tubular cell line HK-2. Cobalt chloride treatment significantly increased the mRNA expression of not only glucose transporter 1 (GLUT1), a typical HIF-1 target gene mRNA, but also ABCG2 mRNA in HK-2 cells. The BCRP inhibitor Ko143-sensitive accumulation of BCRP substrates such as Hoechst33342 and mitoxantrone was significantly enhanced by cobalt chloride treatment. In addition, treatment with cobalt chloride significantly increased the Ko143-sensitive accumulation of fluorescein isothiocyanate-labeled methotrexate in HK-2 cells. Furthermore, cobalt chloride treatment attenuated the cytotoxicity induced by mitoxantrone and methotrexate, which might be, at least in part, due to the increase in BCRP-mediated transport activity via HIF-1 activation. These findings indicate that HIF-1 activation protects renal proximal tubular cells against BCRP substrate-induced cytotoxicity by enhancing the expression and function of BCRP in renal proximal tubular cells.
File Format	HTM / HTML
ISSN	09186158
e-ISSN	13475215
Journal	Biological & Pharmaceutical Bulletin
Issue Number	1
Volume Number	40
Language	English
Publisher	The Pharmaceutical Society of Japan J-STAGE
Publisher Date	2017-01-01
Publisher Place	Japan
Access Restriction	Open
Subject Keyword	Discipline Biochemistry Discipline Pharmacology Metabolism Cobalt Pharmacology Epithelial Cells Drug Effects Neoplasm Proteins Genetics Cell Line Cell Survival Glucose Transporter Type 1 Hypoxia-inducible Factor 1, Alpha Subunit Methotrexate Mitoxantrone Rna, Messenger
Content Type	Text
Resource Type	Article
Subject	Medicine Pharmacology Pharmaceutical Science

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