【摘要】 目的在胰腺癌治疗中,吉西他滨的化疗耐受机制目前仍不清楚。文中探讨miR-100对胰腺癌患者吉西他滨化疗敏感性的影响及作用机制。方法通过实时荧光定量PCR和Western blot检测miR-100对PLK1基因水平和蛋白水平的影响。利用荧光素酶试验验证PLK1是miR-100的靶基因。通过流式细胞仪检测miR-100对人胰腺癌细胞株SW1990吉西他滨敏感性的影响。结果 PCR结果显示,过表达miR-100能够降低PLK1基因水平。Western blot结果显示,过表达miR-100能够使PLKA1蛋白表达降低。荧光素酶试验结果显示,miR-100能够显著降低PLK1-3’-UTR质粒的荧光素活性。流式细胞仪结果显示,过表达miR-100能使细胞凋亡率明显升高。结论 miR-100能提高人胰腺癌细胞株SW1990对吉西他滨的敏感性,miR-100抑制PLK1的表达可能是其作用机制。更多还原

【Abstract】 Objective The mechanism of gemcitabine chemotherapy tolerance in the treatment of pancreatic cancer remains unclear. This study is to investigate the effect of miR-100 on gemcitabine sensitivity of pancreatic cancer and its mechanism. Methods The effects of miR-100 on the expressions of PLK1 mRNA and protein were detected by quantitative real time PCR and Western-blot. PLK1 was confirmed to be a target gene of miR-100 by luciferase assay. The effect of miR-100 on gemcitabine sensitivity of human pancreatic cancer cell line SW1990 was determined by flow cytometry. Results The overexpression of miR-100 markedly reduced the level of PLK1 mRNA and that of the PLKA1 protein,but increased the apoptosis of pancreatic cancer cells. The luciferase activity of the PLK1-3’-UTR plasmid was significantly suppressed by miR-100. Conclusion miR-100 improves the gemcitabine sensitivity of the human pancreatic cancer cell line SW1990,which may be associated with its inhibitory effect on PLK1.更多还原