TrkA-siRNA增强人乳腺癌MCF-7细胞对紫杉醇的敏感性

目的 探讨靶向抑制TrkA基因表达后,人乳腺癌细胞MCF-7对化疗药物紫杉醇敏感性的变化.方法 8 μmol/L紫杉醇作用于乳腺癌MCF-7亲本细胞株和TrkA-siRNA转染细胞株24、48小时后,MTT法检测细胞增殖抑制效应,Western blot检测凋亡蛋白caspase-3的活化.倒置显微镜观察细胞株生长的形态学变化.结果 紫杉醇作用24、48小时后,其对TrkA-siRNA细胞株的生长抑制均高于MCF-7亲本细胞株(P＜0.05),且48小时抑制率高于24小时(P＜0.05).Western blot结果显示,caspase-3蛋白在紫杉醇作用24小时后被激活,其在TrkA-siRNA细胞株中的表达高于MCF-7亲本细胞株(P＜0.05).结论 TrkA-siRNA能增加乳腺癌细胞对化疗药物紫杉醇的敏感性.

TrkA-siRNA enhances chemosensitivity to paclitaxel in human breast cancer MCF-7 cells

Objective To investigate the effect of TrkA-siRNA on chemosensitivity to paclitaxel in human breast cancer MCF-7 cells. Methods Breast cancer MCF-7 cells were transfected with TrkA-siRNA. Parent MCF-7 cells and transfected MCF-7 cells were treated with paclitaxel of 24 h and 48 h in vitro. Cell proliferation was measured by MTr assay. The expression of caspase-3 protein was detected by Western blot. The morphological change was observed under an inverted microscope. Results Cell proliferation in transfected cells was significantly inhibited compared to that in parent cells after paclitaxel treatment for 24 h and 48 h （ P 〈 0.05 ）. The expression of caspase-3 protein in transfected cells was higher than that in parent cells after treated with paclitaxel for 24 h （ P 〈 0.05 ）. Conclusion TrkA-siRNA can enhance chemosensitivity to paclitaxel in human breast cancer MCF-7 cells.