摘要
目的探讨血管内皮生长因子(VEGF)mRNA干扰对乳腺癌的治疗意义。方法应用RNA干扰技术,对乳腺癌细胞株MCF-7进行VEGF mRNA干扰,并辅以放、化疗处理。在干扰前后用流式细胞技术、MTT比色法等技术对MCF-7细胞株的细胞周期、凋亡率、抑制率进行检测。结果流式细胞技术显示,转染VEGF siRNA后MCF-7细胞出现G0-G1阻滞(F=15.237,P=0.017)、凋亡明显增加(F=11.160,P=0.029);MTT比色法发现,转染前后,紫杉醇对MCF-7细胞的抑制效率明显提高(F=5.256,P=0.036),作用转染前后MCF-7细胞48h IC50分别为4.76 mmol/L、3.29 mmol/L;克隆形成率实验中,MCF-7细胞经转染后,克隆形成率出现明显下降,并对紫杉醇及放射治疗具有明显的协同作用(P<0.05)。结论 VEGF基因干扰可以抑制MCF-7细胞的增殖、促进其凋亡,并能提高MCF-7细胞对放化疗的敏感性。
Objective To explore VEGFmRNA interference on the treatment of breast cancer significance. Method After knockdown of VEGFmRNA expression using VEGF shRNA, breast cancer MCF-7 cell were treated with chemotherapy or radiotherapy or chemotherapy plus radiotherapy or without any treatment. We investigated the changes in cell cycle, apoptosis rate, and cell colony-formation,Results After knockdown of VEGFmRNA expression using VEGF shRNA, VEGF mRNA levels in breast cancer MCF-7 cell were inhibited significantly （ P 〈 0.01 ）. The flow cytometric data showed that both control cells and VEGF shRNA-transfected cells exhibited G0-G1 arrest （ F = 15. 237, P = 0. 017 ）, reduced number of cell in the G2 and M phases. The apoptosis rate of VEGF shRNA-transfected cells increased compared to the control cells（ F = 11. 160 ,P = 0. 029）. We found VEGF knockdown significantly sensitized MCF-7 cells to paclitaxel （ F = 5. 256, P = 0.036 ）. After VEGF knockdown, colony formation in paclitaxel and radiation treated MCF-7 cells was significantly reduced （ P 〈 0.05 ）, Conclusion VEGF gene expression interference can inhibit the proliferation of MCF-7 cells and promote MCF-7 cells apoptosis, and increase the sensitivity of chemotherapy and radiotherapy.
出处
《中国临床保健杂志》
CAS
2013年第3期295-298,F0003,共5页
Chinese Journal of Clinical Healthcare
关键词
乳腺肿瘤
血管内皮生长因子类
RNA
信使
转染
紫杉酚
Breast neoplasms
Vascular endothelial growth factors
RNA, messenger
Transfection
Paclitaxel
