Institute of Genetic Engineering, Southern Medical University, Guangzhou, Peoples Republic of China.
Cell Biol Int. 2012 Jul;36(7):653-9. doi: 10.1042/CBI20100918.
The oncogene, microRNA-155, is significantly elevated in GBM (glioblastoma multiforme), regulating multiple genes associated with cancer cell proliferation, apoptosis and invasiveness. Thus, miR-155 can theoretically become a target for enhancement of the chemotherapy in cancer. Down-regulating miR-155 to enhance the effect of taxol has not been studied in human GBM. Human GBM U251 cells were treated with taxol and the miR-155 inhibitor alone or in combination. IC50 values were dramatically decreased in cells treated with miR-155 inhibitor combined with taxol, to a greater extent than those treated with taxol alone. Furthermore, the miR-155 inhibitor significantly enhanced apoptosis in U251 cells. The data suggest that miR-155 blockage increased the chemosensitivity to taxol in GBM cells, making combined treatment an effective therapeutic strategy for controlling the growth by inhibiting EAG1 expression.
致癌基因 microRNA-155 在 GBM(多形性胶质母细胞瘤)中显著升高,调节与癌细胞增殖、凋亡和侵袭相关的多个基因。因此,miR-155 理论上可以成为增强癌症化疗效果的靶点。下调 miR-155 以增强紫杉醇的作用尚未在人类 GBM 中进行研究。用紫杉醇和 miR-155 抑制剂单独或联合处理人 GBM U251 细胞。用 miR-155 抑制剂联合紫杉醇处理的细胞的 IC50 值显著降低,程度大于单独用紫杉醇处理的细胞。此外,miR-155 抑制剂显著增强了 U251 细胞的凋亡。数据表明,miR-155 阻断增加了 GBM 细胞对紫杉醇的化疗敏感性,使联合治疗成为通过抑制 EAG1 表达来控制肿瘤生长的有效治疗策略。