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反义 miR-155 寡核苷酸通过诱导细胞凋亡增强 U251 细胞对紫杉醇的化疗敏感性。

Anti-miR-155 oligonucleotide enhances chemosensitivity of U251 cell to taxol by inducing apoptosis.

机构信息

Institute of Genetic Engineering, Southern Medical University, Guangzhou, Peoples Republic of China.

出版信息

Cell Biol Int. 2012 Jul;36(7):653-9. doi: 10.1042/CBI20100918.

Abstract

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.

摘要

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。

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