摘要
目的观察紫杉醇对人甲状腺未分化癌DRO细胞增殖、细胞凋亡以及血管内皮生长因子(VEGF)、bcl-2和bax基因表达的影响。方法MTT法检测紫杉醇对DRO细胞增殖的抑制效应;流式细胞术检测经紫杉醇6.25μg/L作用24、487、2 h后细胞周期和凋亡率的变化;RT-PCR方法观察经紫杉醇6.25μg/L作用48 h后细胞内VEGF、bcl-2和bax基因的表达情况。结果紫杉醇能够抑制DRO细胞生长,72 h的IC50为10μg/L;可将细胞阻滞于G2/M期并诱导其凋亡,6.25μg/L紫杉醇作用48 h后凋亡达高峰,凋亡率为32.76%±1.54%;细胞内VEGF的表达低于对照组;凋亡抑制基因bcl-2在细胞凋亡过程中表达没有显著性变化,而促凋亡基因bax呈高表达。结论紫杉醇明显抑制DRO细胞生长,并诱导细胞凋亡,且能下调VEGF的表达,bax基因在紫杉醇诱导的DRO细胞凋亡中可能起着重要的调控作用。
Objective To investigate the effect of paclitaxel on the growth of human anaplasfic thyroid carcinoma cell line in vitro. Methods Human anaplastic thyroid carcinoma DRO cell line was treated with paclitaxel of different concentrations and for varied length of acting time. The antiprolifemtive effect was measured by methyl tb.Jazolyl tetrazolium （MTT）. Flow cytometry was used to examine apoptosis and cell cycle when paclitaxel was 6.25 μg/L in concentration and the exposure to DRO was 24 h, 48 h and 72 h respectively. The levels of VEGF mRNA, bcl - 2 mRNA and bax mRNA in cells were detected by RT - PCR, with paclitaxel at 6.25 μg/L for 48 h. Results Paclitaxel had marked suppressive effect on the growth of DRO cell line, with the IC50 value being 10 μg/L after 72 h of incubation with paclitaxel. Paclitaxel could arrest the cell cycle at G2/M stage and induce apoptosis. Apoptosis peaked after 48 h of incubation with 6.25 μg/L paclitaxel, with the apoptosis rate being 32.76% - 1.54%. The VEGF mRNA in paclitaxel group was less than in the control group. The expression of bcl - 2 mRNA was not altered, while that of bax mRNA was increased after paclitaxel treatment. Conclusion Paclitaxd can significantly inhibit the proliferation, induce apoptosis and decrease the expression of VEGF of DRO cells. The altered expression of bax gene might play an important role in regulating paclitaxel- induced apoptosis.
出处
《徐州医学院学报》
CAS
2006年第6期474-477,共4页
Acta Academiae Medicinae Xuzhou
基金
江苏省卫生厅135工程资助项目(2001031)
关键词
紫杉醇
甲状腺未分化癌
细胞凋亡
paclitaxel
anaplastic thyroid carcinoma
apoptosis
