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作 者:肖建英[1] 李男[1] 张秀梅[1] 赵颂[1] 王翠瑶[1] 崔明宇[1]
出 处:《肿瘤防治研究》2010年第7期759-762,共4页Cancer Research on Prevention and Treatment
基 金:辽宁省自然科学基金资助项目(20062201)
摘 要:目的观察全反式维甲酸(ATRA)对甲状腺鳞癌SW579细胞株生长增殖及维甲酸受体β(RARβ)和p21表达的影响,进而探讨维甲酸的抗癌作用机制。方法甲状腺鳞癌SW579细胞株经不同浓度ATRA作用48h后,在倒置显微镜下观察细胞生长情况及形态变化;MTT法测定细胞增殖活性;流式细胞仪检测细胞周期;RT-PCR方法检测细胞RARβ及p21mRNA的表达。结果随着ATRA的升高,SW579细胞的生长呈显著抑制状态,细胞生长滞留在G1期,RARβ和p21mRNA表达水平均显著上调,呈剂量依赖性。结论 ATRA在一定浓度范围内对甲状腺鳞癌SW579细胞株有剂量依赖性的增殖抑制作用,其机制可能与提高细胞RARβ基因的表达、进而再上调p21的表达有关。Objective To observe the effects of all-trans-retinoic acid(ATRA) on the expression of RARβ and p21 gene and also proliferation of thyroid squamous cell carcinoma cell line (SW579)so as to explore its mechanism.Methods The cells were randomly divided into control group and ATRA groups.ATRA groups were treated with different dose of ATRA respectively (final concentration of 10^-7 mol/L、5×10^-7 mol/L、10^-6 mol/L、5×10^-6 mol/L、10^-5 mol/L).24 hours later,ATRA at different concertrations were added.Treated with ATRA for 48 hours,the growth and shape of the cells were observed with a convert microscope.The proliferation of the cells was observed with MTT and the cell cycle was measured by flow cytometry;The mRNA expression levels of RARβ and p21 were determined by RT-PCR.Results After cells were treated with ATRA at low concentration respectively,the malignant phenotypes of cells gradually changed to the mature cells.At high concentration groups cells changed unremarkably.The proliferation index decreased markedly with a dose-dependent manner.Flow cytometry analysis showed the percent of G1 phase cells was significantly higher than that of the control groups and the percent of S phase cells was lower than that of the control groups.The cell cycle was arrested at G1 stage.The expression of the RARβ and p21 mRNA increases dramatically with ATRA at different concentrations.Conclusion ATRA can inhibit the proliferation of thyroid squamous cell carcinoma cell line with a dose-dependent manner,and the mechanism of which may be related to increases of RARβ and p21 mRNA expression.
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