Department of Radiotherapy, University Hospital Essen, Essen, Germany.
Institute of Cell Biology, University Hospital Essen, Essen, Germany.
Sci Rep. 2019 Feb 4;9(1):1282. doi: 10.1038/s41598-018-38004-5.
Cisplatin is an extensively used chemotherapeutic drug for lung cancer, but the development of resistance decreases its effectiveness in the treatments of non-small cell lung cancer (NSCLC). In this study, we examined the effects of metformin, a widely used antidiabetic drug, on cisplatin radiosensitization in NSCLC cell lines. Human NSCLC cell lines, A549 (cisplatin-resistant) and H460 (cisplatin-sensitive), were treated with metformin, cisplatin or a combination of both drugs before ionizing radiation. Cell proliferation, clonogenic assays, western blotting, cisplatin-DNA adduct formation and immunocytochemistry were used to characterize the treatments effects. Metformin increased the radiosensitivity of NSCLC cells. Metformin showed additive and over-additive effects in combination with cisplatin and the radiation response in the clonogenic assay in H460 and A549 cell lines (p = 0.018 for the interaction effect between cisplatin and metformin), respectively. At the molecular level, metformin led to a significant increase in cisplatin-DNA adduct formation compared with cisplatin alone (p < 0.01, ANOVA-F test). This was accompanied by a decreased expression of the excision repair cross-complementation 1 expression (ERCC1), a key enzyme in nucleotide excision repair pathway. Furthermore, compared with each treatment alone metformin in combination with cisplatin yielded the lowest level of radiation-induced Rad51 foci, an essential protein of homologous recombination repair. Ionizing radiation-induced γ-H2AX and 53BP1 foci persisted longer in both cell lines in the presence of metformin. Pharmacological inhibition of AMP-activated protein kinase (AMPK) demonstrated that metformin enhances the radiosensitizing effect of cisplatin through an AMPK-dependent pathway only in H460 but not in A549 cells. Our results suggest that metformin can enhance the effect of combined cisplatin and radiotherapy in NSCLC and can sensitize these cells to radiation that are not sensitized by cisplatin alone.
顺铂是一种广泛用于治疗肺癌的化疗药物,但耐药性的发展降低了其在非小细胞肺癌(NSCLC)治疗中的效果。在这项研究中,我们研究了广泛使用的抗糖尿病药物二甲双胍对 NSCLC 细胞系中顺铂放射增敏的影响。人 NSCLC 细胞系 A549(顺铂耐药)和 H460(顺铂敏感)在接受电离辐射前用二甲双胍、顺铂或两者联合处理。细胞增殖、集落形成实验、western blot、顺铂-DNA 加合物形成和免疫细胞化学用于描述治疗效果。二甲双胍增加了 NSCLC 细胞的放射敏感性。二甲双胍与顺铂联合使用在 H460 和 A549 细胞系中的集落形成实验中表现出相加和超相加的作用(顺铂和二甲双胍之间的相互作用效应,p = 0.018)。在分子水平上,与单独使用顺铂相比,二甲双胍导致顺铂-DNA 加合物的形成显著增加(p < 0.01,ANOVA-F 检验)。这伴随着切除修复交叉互补 1 表达(ERCC1)的表达减少,ERCC1 是核苷酸切除修复途径中的关键酶。此外,与单独使用每种药物相比,二甲双胍与顺铂联合使用产生的同源重组修复所必需的蛋白质辐射诱导的 Rad51 焦点最低。在存在二甲双胍的情况下,两种细胞系中的电离辐射诱导的 γ-H2AX 和 53BP1 焦点持续时间更长。AMP 激活蛋白激酶(AMPK)的药理学抑制表明,二甲双胍仅在 H460 细胞中通过 AMPK 依赖性途径增强顺铂的放射增敏作用,而在 A549 细胞中则没有。我们的结果表明,二甲双胍可以增强 NSCLC 中顺铂联合放疗的效果,并使这些细胞对单独顺铂不敏感的辐射敏感。