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目的:观察曲古抑菌素A(TSA)对甲状腺未分化癌DRO细胞株的体外作用,探讨TSA对甲状腺未分化癌的作用机制。方法:倒置相差显微镜观察细胞形态变化;MTT法检测TSA对DRO细胞增殖的抑制效应;流式细胞术检测经TSA1.0μmol/L作用24、48、72h后细胞周期和凋亡率的变化;RT-PCR方法观察经TSA1.0μmol/L作用48h后细胞内hTERT和p21基因的表达情况。结果:在0.1～1.5μmol/LTSA作用下,DRO细胞生长明显受抑制;倒置相差显微镜检测DRO细胞经TSA处理后形态发生明显变化;1.0μmol/LTSA作用于DRO细胞,48h后出现明显的细胞周期阻滞;hTERT经TSA诱导后表达明显下调,呈量效关系。结论:一定浓度的TSA可以抑制甲状腺未分化癌细胞株DRO增殖。其作用机制可能与下调hTERT表达有关。
Objective: To observe the effect of trichostatin A (TSA) on human undifferentiated thyroid carcinoma cell line DRO and to explore the mechanism of TSA on human undifferentiated thyroid carcinoma. Methods: The morphological changes of cells were observed by inverted phase contrast microscope. The inhibitory effect of TSA on the proliferation of DRO cells was detected by MTT assay. The cell cycle and apoptosis rate were detected by flow cytometry at 24, 48 and 72 h after treatment with TSA 1.0 μmol / L. -PCR method was used to observe the expression of hTERT and p21 gene in TSH1.0μmol / L treated cells for 48h. Results: Under the action of 0.1 ~ 1.5μmol / L TSA, the growth of DRO cells was obviously inhibited. The morphological changes of DRO cells were detected by inverted phase contrast microscope. After treated with 1.0μmol / L TSA for DRO cells, obvious cell cycle appeared HTERT was downregulated after TSA induction, showing a dose-response relationship. Conclusion: A certain concentration of TSA can inhibit the proliferation of thyroid undifferentiated carcinoma cell line DRO. Its mechanism may be related to down-regulation of hTERT expression.