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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Metformin Inhibits Proliferation and Tumor Growth of QGP-1 Pancreatic Neuroendocrine Tumor Cells by Inducing Cell Cycle Arrest and Apoptosis
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Metformin Inhibits Proliferation and Tumor Growth of QGP-1 Pancreatic Neuroendocrine Tumor Cells by Inducing Cell Cycle Arrest and Apoptosis

机译：二甲双胍通过诱导细胞周期停滞和细胞凋亡来抑制QGP-1胰腺神经内分泌肿瘤细胞的增殖和肿瘤生长

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Background/Aim: Pancreatic neuroendocrine tumors (pNETs) are rare pancreatic neoplasms, and therapeutic options for pNETs are limited. Metformin is an anti- hypoglycemic drug that appears to have anticancer effects. However, little is known about the effect of metformin on pNETs. In this study, we investigated the anti-proliferative effect of metformin on a human pNET cell line. Materials and Methods: The anti-proliferative properties of metformin were evaluated in QGP-1 and NCI-H727 cells using a cell counting kit-8 assay. Xenograft mouse models were used to assess the tumor effect in vivo. Results: Metformin inhibited the proliferation and anti-tumor growth of QGP-1 cells, accompanied by their arrest during the cell cycle at the G0/G1 phase. Immunohistochemical analysis of tumor tissues revealed down-regulation of cyclin D1 and proliferating cell nuclear antigen in the metformin-treated group. Additionally, metformin induced apoptosis, and the expression of survivin and claspin were decreased in metformin-treated QGP- 1 cells according to the apoptosis array. Furthermore, the angiogenic related protein TIMP-1 was down-regulated, and its miRNA expression was altered by metformin in QGP- 1 cells. Conclusion: Taken together, our study demonstrated the therapeutic potential of metformin and provides molecular mechanistic insights into its anti-tumoral effect on pNETs. This study is the first one describing anti-tumoral effects in pNETs.
机译：背景/目的：胰腺神经内分泌肿瘤（PNets）是罕见的胰腺肿瘤，PNets治疗选择有限。二甲双胍是一种似乎具有抗癌效果的抗低血糖药物。然而，关于二甲双胍对PNets的影响很少。在这项研究中，我们研究了二甲双胍对人PNET细胞系的抗增殖作用。材料和方法：使用细胞计数试剂盒-8测定法在QGP-1和NCI-H727细胞中评价二甲双胍的抗增殖性质。异种移植鼠标模型用于评估体内肿瘤作用。结果：二甲双胍抑制QGP-1细胞的增殖和抗肿瘤生长，在G0 / G1相的细胞周期中伴有它们的停滞。肿瘤组织的免疫组织化学分析显示了二甲双胍治疗组细胞周期蛋白D1和增殖细胞核抗原的下调。另外，根据细胞凋亡阵列，二甲双胍处理的QGP-1细胞中，Survivin和Claspin的表达和Survivin和Claspin的表达减少。此外，血管生成相关蛋白质TIMP-1被下调，其miRNA表达通过QGP-1细胞中的二甲双胍改变。结论：综合，我们的研究表明二甲双胍的治疗潜力，并为其对PNets的抗肿瘤作用提供分子机制见解。本研究是第一个描述PNets中抗肿瘤作用的第一个。

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