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Metformin induces apoptosis via a mitochondria-mediated pathway in human breast cancer cells in vitro

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Breast cancer is the most commonly occurring cancer and second leading cause of mortality in women. Metformin is a widely prescribed anti-hyperglycemic drug, which is emerging as a potential cancer preventative and treatment agent. However, the mechanisms underlying the suppressive effects of metformin on cancer cell growth and the induction of cancer cell apoptosis are not fully elucidated. The present study aimed to identify the pathways regulated by metformin in two breast cancer cell lines, MDAMB231 and MDAMB435. Cells were treated with various concentrations of metformin and then evaluated with respect to viability, proliferation, adenosine triphosphate (ATP) and reactive oxygen species (ROS) levels, mitochondrial membrane potential (Δψm), and the expression of anti and proapoptotic proteins. Metformin caused apoptosis in a concentration and timedependent manner, and decreased cell viability and ATP production. Furthermore, metformin induced the generation of ROS and decreased the Δψm. Moreover, metformin downregulated the expression of the antiapoptotic proteins Bcell lymphoma 2 (BCL2) and myeloid cell leukemia1, and upregulated the expression of the proapoptotic BCL2associated X protein in MDAMB231 cells. These results demonstrate that the apoptotic and cytotoxic effects of metformin on breast cancer cells are mediated by the intrinsic mitochondria-mediated apoptosis pathway.
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Document Type: Research Article

Affiliations: 1: Department of Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230032. P.R. China 2: Faculty of Pharmacy, Bengbu Medical College, Anhui Engineering Technology Research Center of Biochemical Pharmaceuticals, Bengbu, Anhui 233030, P.R. China 3: Department of Oncology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233022, P.R. China

Publication date: January 1, 2016

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  • Experimental and Therapeutic Medicine aims to ensure the expedient publication, in both print and electronic format, of studies relating to biology, gene therapy, infectious disease, microbiology, molecular cardiology and molecular surgery. The journal welcomes studies pertaining to all aspects of molecular medicine, and studies relating to in vitro or in vivo experimental model systems relevant to the mechanisms of disease are also included.

    All materials submitted to this journal undergo the appropriate review via referees who are experts in this field. All materials submitted follow international guidelines with regard to approval of experiments on humans and animals.
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