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目的:研究microRNA-7(miR-7)对非小细胞肺癌A549和H1299细胞表柔比星(epirubicin,EPI)化疗的增敏作用及其机制。方法:EPI、miR-7 mimics单独或联合处理A549和H1299细胞后,CCK-8法检测A549和H1299细胞的增殖,Annexin-V/PI染色流式细胞术检测A549和H1299细胞的凋亡,实时定量PCR检测A549和H1299细胞中EGFR及Raf-1mRNA的表达。结果:单独使用EPI或转染miR-7 mimics均可抑制A549和H1299细胞的增殖(P<0.05),而转染miR-7 mim-ics后再以50～400 ng/ml EPI处理,较单独EPI处理显著增强对A549和H1299细胞增殖的抑制作用(P<0.05)。当miR-7mimics与EPI联用时,A549和H1299细胞的凋亡率则分别较EPI单独处理组增加(54.9±0.4)%和(67.2±0.5)%(均P<0.01),且伴随EGFR及Raf-1 mRNA表达量的显著下降(P<0.01),A549细胞中分别降低(68.0±6.0)%和(78.2±3.9)%,H1299细胞中分别降低(94.8±6.2)%和(87.8±4.3)%。结论:miR-7可通过下调EGFR及Raf-1 mRNA的表达,协同EPI抑制非小细胞肺癌A549和H1299细胞的增殖,并促进细胞凋亡。
Objective: To study the sensitizing effect of microRNA-7 (miR-7) on epirubicin (EPI) chemotherapy in non-small cell lung cancer A549 and H1299 cells and its mechanism. Methods: A549 and H1299 cells were treated with EPI and miR-7 mimics alone or in combination. CCK-8 assay was used to detect the proliferation of A549 and H1299 cells. Annexin-V / PI staining was used to detect the apoptosis of A549 and H1299 cells. Real- Quantitative PCR was used to detect the expression of EGFR and Raf-1mRNA in A549 and H1299 cells. Results: The proliferation of A549 and H1299 cells was inhibited by EPI alone or transfected with miR-7 mimics (P <0.05), while those treated with EPI at 50-400 ng / ml after miR-7 mim-ics were transfected EPI treatment significantly inhibited the proliferation of A549 and H1299 cells (P <0.05). When miR-7mimics was used in combination with EPI, the apoptotic rates of A549 and H1299 cells were (54.9 ± 0.4)% and (67.2 ± 0.5)% higher than those of EPI alone group (all P <0.01) (94.8 ± 6.2)% and (87.8 ± 4.3)% in H1299 cells decreased significantly (68.0 ± 6.0) and (78.2 ± 3.9)% in A549 cells, %. Conclusions: miR-7 can inhibit the proliferation of non-small cell lung cancer A549 and H1299 cells and promote cell apoptosis by down-regulating the expression of EGFR and Raf-1 mRNA.