Effect of amlodipine on apoptosis of human breast carcinoma MDA-MB-231 cells

Objective： To elucidate the effects of amlodipine on the proliferation and apoptosis of human breast carcinoma MDA-MB-231 cells. Methods： Light microscopy was used to determine the effects of amlodipine on cell morphology; Flow cytometry was used to quantitate cells undergoing apoptosis; the expression of a cell cycle-related protein, proliferating cell nuclear antigen （PCNA） and an antiapoptosis protein, Bcl-2 were assessed by immunocytochemistry. Results： Amlodipine concentration of 8.25umol/L （1/2 of ICs0） affected the morphology, decreased the expression of PCNA and Bcl-2 and induced apoptosis of human breast carcinoma MDA-MB-231 cells. Conclusion： The effect of amlodipine on the antiproliferation of human breast carcinoma MDA-MB-231 cells is related to inducement of apoptosis, and the decrease of the expression of Bcl-2 and PCNA may be the possible mechanism for proliferation inhibitory and inducement of apoptosis.

基底样乳腺癌中微小RNA-205靶向调控KLF12以及对MDA—MB-468细胞凋亡的影响

目的 观察基底样乳腺癌（BLBC）特异性微小RNA（miRs）及其靶基因和生物学功能。方法通过荧光素酶实验验证靶基因，逆转录定量-聚合酶链反应（QRT-PCR）、Western印迹和免疫组织化学（IHC）分析miR及其靶基因表达，流式细胞检测细胞凋亡。结果荧光素酶实验示miR-205靶向调控KLF12（P＝0.001 6）。QRT-PCR示，miR-205在MDA-MB-468细胞（P＝0.007）和BLBC肿瘤组织中（P＝0.007 4；n＝3）呈低表达；KLF12在MDA-MB-468细胞中为高表达（P＝0.003 9）；过表达miR-205，miR-205在MDA-MB-468表达显著升高（P＝0.000），KLF12在MDA-MB-468表达显著减少（P＝0.038）。Western印迹示BLBC肿瘤组织中KLF12蛋白表达显著升高（P＝0.008 3；n＝9）。凋亡实验示过表达miR-205，显著促进MDA-MB-468细胞凋亡（P＝0.0061）。结论MiR-205是BLBC特异性miR，通过负性靶向调控原癌基因KLF12和促进细胞凋亡具有抑癌基因的功能。MiR-205和KLF12为BLBC提供潜在的诊断分子标志物和新的治疗思路。

杠柳毒苷体外抑制肝癌细胞和乳腺癌细胞增殖的实验研究

目的探讨杠柳毒苷在体外对人乳腺癌MDA-MB-468细胞和人肝癌HepG2细胞增殖的影响。方法 MTT法观察杠柳毒苷对人乳腺癌MDA-MB-468细胞和人肝癌HepG2细胞增殖的抑制作用,流式细胞术观察杠柳毒苷对两种肿瘤细胞的细胞增殖周期作用。结果与对照组比较,杠柳毒苷能明显抑制两种肿瘤细胞的增殖,其抑制率与药物浓度和作用时间呈正相关。流式细胞仪检测发现,杠柳毒苷对乳腺癌MDA-MB-468细胞和肝癌HepG2细胞持续作用24 h后,可以使G0/G1期细胞增多,G2/M期细胞减少。结论杠柳毒苷具有抑制乳腺癌MDA-MB-468细胞和肝癌HepG2细胞增殖的作用,并可将乳腺癌MDA-MB-468细胞和肝癌HepG2细胞的细胞生长周期阻滞在G0/G1期。