Pierro J, Saba C, McLean K, Williams R, Karpuzoglu E, Prater R, Hoover K, Gogal R
University of Georgia, College of Veterinary Medicine, Department of Small Animal Medicine and Surgery, 2200 College Station Road, Athens, GA 30602, United States.
University of Georgia, College of Veterinary Medicine, Department of Small Animal Medicine and Surgery, 2200 College Station Road, Athens, GA 30602, United States.
Res Vet Sci. 2017 Oct;114:74-79. doi: 10.1016/j.rvsc.2017.03.003. Epub 2017 Mar 6.
Metformin is an oral hypoglycemic drug that has been shown to inhibit cancer cell proliferation via up-regulation of AMPK (AMP-activated protein kinase), and possibly inhibition of mTOR (mammalian target of rapamycin). The purpose of this study was to evaluate the effects of metformin on a feline injection site sarcoma cell line. Cells from a feline injection site sarcoma cell line were treated with metformin at varied concentrations. A dose-dependent decrease in cell viability following metformin treatment was observed, with an IC50 of 8.0mM. Using flow cytometry, the mechanism of cell death was determined to be apoptosis or necrosis. To evaluate the role of mTOR inhibition in metformin-induced cell death, Western blot was performed. No inhibition of mTOR or phosphorylated mTOR was found. Although metformin treatment leads to apoptotic or necrotic cell death in feline injection site sarcoma cells, the mechanism does not appear to be mediated by mTOR inhibition.
二甲双胍是一种口服降糖药，已被证明可通过上调AMPK（AMP激活的蛋白激酶）来抑制癌细胞增殖，并可能抑制mTOR（雷帕霉素的哺乳动物靶点）。本研究的目的是评估二甲双胍对猫注射部位肉瘤细胞系的影响。用不同浓度的二甲双胍处理猫注射部位肉瘤细胞系的细胞。观察到二甲双胍处理后细胞活力呈剂量依赖性下降，IC50为8.0mM。使用流式细胞术确定细胞死亡机制为凋亡或坏死。为了评估mTOR抑制在二甲双胍诱导的细胞死亡中的作用，进行了蛋白质免疫印迹分析。未发现mTOR或磷酸化mTOR受到抑制。虽然二甲双胍处理导致猫注射部位肉瘤细胞发生凋亡或坏死性细胞死亡，但其机制似乎不是由mTOR抑制介导的。
