靶向ABCB1的siRNA增强了人三阴性乳腺癌细胞化疗的疗效

Goknur Kara
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摘要

多药耐药(MDR)导致化疗效果降低是三阴性乳腺癌(TNBC)的主要临床问题。多药耐药的发生通常是由于atp结合盒B1 (ABCB1)蛋白的过表达,该蛋白从癌细胞中渗出各种抗癌药物。通过RNA干扰(RNA interference, RNAi)敲低ABCB1基因是解决MDR的新技术之一。RNAi是一种基因沉默过程,小干扰RNA (small interfering RNA, siRNA)以高效率/特异性阻断所需基因的表达。这项工作的目的是研究通过特定sirna抑制ABCB1对紫杉醇或依托泊苷在TNBC细胞中的疗效的影响。采用MTT试验评估增加紫杉醇和依托泊苷浓度对MDA-MB-231细胞的毒性。然后将细胞与紫杉醇或依托泊苷联合ABCB1-siRNA共同处理,然后进行细胞毒性、集落形成和迁移试验。与单独使用siRNA或药物相比,ABCB1-siRNA与紫杉醇或etopo苷联合使用显示出协同效应,siRNA-药物治疗显著降低了TNBC细胞的活力、克隆原性和迁移。总之,这些结果表明,在ABCB1-siRNA转染后,TNBC细胞即使对亚毒性剂量的紫杉醇和依托泊苷也变得脆弱,这代表了一种有希望增强化疗对TNBC影响的方法。
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siRNA targeting ABCB1 potentiates the efficacy of chemotherapy in human triple-negative breast cancer cells
Diminishing the efficacy of chemotherapy because of multidrug resistance (MDR) is a major clinical problem for triple-negative breast cancer (TNBC). MDR often occurs by overexpression of ATP-binding cassette B1 (ABCB1) protein that effuses various anticancer drugs from cancer cells. One of the newly developed techniques to addressing MDR is to knockdown ABCB1 by RNA interference (RNAi). RNAi is a gene-silencing process in that small interfering RNA (siRNA) blocks the expression of desired genes with high efficiency/specificity. The aim of this work is to examine the impact of ABCB1 inhibition via specific siRNAs on the efficacy of paclitaxel or etoposide in TNBC cells. The toxicity of increasing paclitaxel and etoposide concentrations on MDA-MB-231 cells was assessed using the MTT test. Cells were then co-treated with paclitaxel or etoposide in combination with ABCB1-siRNA, followed by cytotoxicity, colony formation, and migration assays. The administration of ABCB1-siRNA with paclitaxel or etoposide exhibited a synergistic effect and siRNA-drug treatments markedly reduced viability, clonogenicity, and migration of TNBC cells compared to siRNA or drug alone. Overall, these results indicate that TNBC cells become vulnerable even to sub-toxic doses of paclitaxel and etoposide after ABCB1-siRNA transfection, representing a promising aproach to enhance the influence of chemotherapy in TNBC.
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