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首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Metformin Results in Diametrically Opposed Effects by Targeting Non-Stem Cancer Cells but Protecting Cancer Stem Cells in Head and Neck Squamous Cell Carcinoma
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Metformin Results in Diametrically Opposed Effects by Targeting Non-Stem Cancer Cells but Protecting Cancer Stem Cells in Head and Neck Squamous Cell Carcinoma

机译：二甲双胍通过靶向非干癌细胞但保护头颈部鳞状细胞癌的癌干细胞而产生截然相反的效果

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Cancer stem cells (CSCs) have been shown as a distinct population of cancer cells strongly implicated with resistance to conventional chemotherapy. Metformin, the most widely prescribed drug for diabetes, was reported to target cancer stem cells in various cancers. In this study, we sought to determine the effects of metformin on head and neck squamous cell carcinoma (HNSCC). CSCs and non-stem HNSCC cells were treated with metformin and cisplatin alone, and in combination, and cell proliferation levels were measured through MTS assays. Next, potential targets of metformin were explored through computational small molecule binding analysis. In contrast to the reported effects of metformin on CSCs in other cancers, our data suggests that metformin protects HNSCC CSCs against cisplatin in vitro. Treatment with metformin resulted in a dose-dependent induction of the stem cell genes CD44, BMI-1, OCT-4, and NANOG. On the other hand, we observed that metformin successfully decreased the proliferation of non-stem HNSCC cells. Computational drug–protein interaction analysis revealed mitochondrial complex III to be a likely target of metformin. Based on our results, we present the novel hypothesis that metformin targets complex III to reduce reactive oxygen species (ROS) levels, leading to the differential effects observed on non-stem cancer cells and CSCs.
机译：癌症干细胞（CSC）已显示为与常规化学疗法的耐药性密切相关的独特癌细胞群。据报道，二甲双胍是治疗糖尿病最广泛的处方药，其靶向多种癌症中的癌症干细胞。在这项研究中，我们试图确定二甲双胍对头颈部鳞状细胞癌（HNSCC）的影响。 CSC和非干HNSCC细胞分别用二甲双胍和顺铂处理，并联合使用，并通过MTS测定法测量细胞增殖水平。接下来，通过计算小分子结合分析探索了二甲双胍的潜在靶标。与报道的二甲双胍对其他癌症的CSCs的影响相反，我们的数据表明二甲双胍可在体外保护HNSCC CSC免受顺铂的侵害。用二甲双胍治疗导致干细胞基因CD44，BMI-1，OCT-4和NANOG的剂量依赖性诱导。另一方面，我们观察到二甲双胍成功地降低了非干HNSCC细胞的增殖。计算的药物-蛋白质相互作用分析表明，线粒体复合物III可能是二甲双胍的靶标。基于我们的结果，我们提出了新的假说，即二甲双胍靶向复合物III以降低活性氧（ROS）水平，从而导致在非干癌细胞和CSC上观察到差异作用。

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