4.4 Article

Glucosamine attenuates drug resistance in Mitoxantrone-resistance breast cancer cells

期刊

JOURNAL OF PHARMACY AND PHARMACOLOGY
卷 73, 期 7, 页码 922-927

出版社

OXFORD UNIV PRESS
DOI: 10.1093/jpp/rgaa032

关键词

glucosamine; breast cancer resistance protein (BCRP); epithelial; mesenchymal transition (EMT); breast cancer; mitoxantrone

资金

  1. Research Council at Mashhad University of Medical Sciences, Mashhad, Iran [941541]
  2. Isfahan University of Medical Sciences, Isfahan, Iran [396390]

向作者/读者索取更多资源

The study found that glucosamine has inhibitory effects on the proliferation of human breast cancer cells. In the presence of GlcN, the IC50 values of MCF-7/MX cells to mitoxantrone were significantly reduced. Furthermore, GlcN decreased the expression of BCRP mRNA without affecting EMT-related markers in breast cancer cells.
Objectives This study was aimed at investigating the cytotoxicity and multi-drug resistance (MDR) reversal effect of Glucosamine (GlcN) on resistant BCRP-overexpressing breast cancer MCF-7/MX cells. Methods After confirming the overexpression of BCRP, the cytotoxicity and MDR reversing potential of GlcN on MCF-7/MX mitoxantrone-resistant and MCF-7 sensitive breast cancer cells were assessed via MTT assay. The effects of GlcN on mitoxantrone accumulation were analyzed through flow cytometry. Finally, the expression of BCRP and Epithelial-Mesenchymal Transition (EMT)-related markers following the exposure to GlcN were assessed by real-time RT-PCR. Key findings This study showed that glucosamine had an inhibitory effect on the proliferation of human breast cancer cells. The respective IC50 values for MCF-7/MX cells following exposure to mitoxantrone (MX) in the presence of GlcN (0, 0.5 and 1 mm) for 72 h were 3.61 0.21, 0.598 +/- 0.041 and 0.284 +/- 0.016 mu m, respectively. Furthermore, GlcN reduced the expression of BCRP mRNA without any significant effect on EMT-related markers in breast cancer cells. Conclusions These results proposed that glucosamine as a natural sugar could down regulate the BCRP expression and increased MX cytotoxicity in breast cancer cells.

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