This is an archive of papers published by the staff and faculty of Fox Chase Cancer Center. For questions about content, please contact Talbot Research Library
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Redox-dependent modulation of metformin contributes to enhanced sensitivity of esophageal squamous cell carcinoma to cisplatin
Oncotarget. 2017 Sep 22;8(37) :62057-62068
PMID: 28977926 PMCID: PMC5617486 URL: https://www.ncbi.nlm.nih.gov/pubmed/28977926
AbstractGlutathione is the major intracellular anti-oxidant against reactive oxygen species and serves as a detoxification essential. The anti-diabetic drug metformin has been showed to exert anti-tumor activity via modulation of redox homeostasis. In this study, we provided evidence that metformin inhibits proliferation and induces apoptosis of esophageal squamous cancer cells. Importantly, we found that metformin acts as pro-oxidant via depletion of intracellular glutathione. Co-treatment with metformin reversed the elevated intracellular glutathione induced by cisplatin and therefore enhanced the sensitivity to cisplatin in vitro and in vivo. Taken together, our data indicate that combination of metformin with cisplatin may represent a novel therapeutic strategy for esophageal squamous cell carcinoma treatment.
Notes1949-2553 Li, Pin Dong Liu, Zhao Cheng, Tian Tian Luo, Wen Guang Yao, Jing Chen, Jing Zou, Zhen Wei Chen, Li Li Ma, Charlie Dai, Xiao Fang Journal Article United States Oncotarget. 2017 Jul 1. doi: 10.18632/oncotarget.18907.