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作 者:吴洪玉[1] 龚燕芳[1] 徐岷[2] 张玉琦[1] 高道键[1] 李兆申[1] 高军[1]
机构地区:[1]上海长海医院消化科,200433 [2]江苏大学附属医院消化科
出 处:《中华消化杂志》2009年第1期38-41,共4页Chinese Journal of Digestion
摘 要:目的观察曲古菌素A(TSA)对人胃癌细胞株SGC-7901细胞增殖及细胞周期的影响,探讨其可能的机制。方法TSA干预人胃癌SGC-7901细胞24h后,采用四甲基偶氮唑盐法检测其对细胞增殖的影响,流式细胞技术检测细胞周期,实时PCR检测细胞周期素D1和p21 mRNA的表达情况。结果经TSA干预24h后,人胃癌SGC-7901细胞增殖受抑制,TSA0.1、0.5和2.0μmol/L组抑制率分别为3.52%±6.11%、13.29%±4.13%和14.24%±2.80%;同时TSA0.5μmol/L组(71.26%±0.51%)和TSA2.0μmol/L组(71.03%±0.12%)的G0/G1期细胞比例明显高于对照组(51.12%±1.17%);TSA0.5μmol/L组(13.55%±0.44%)和TSA2.0μmol/L组(10.63%±0.63%)的S期细胞比例明显低于对照组(34.60%±0.60%),出现G0/G1细胞周期阻滞。TSA干预后细胞周期相关基因细胞周期素D1 mRNA表达下调和p21 mRNA表达上调。结论TSA通过调控细胞周期相关基因细胞周期素D1和p21的表达,抑制人胃癌SGC-7901细胞的增殖,引起G0/G1期细胞周期阻滞,最终影响肿瘤细胞的生长。Objective To investigate the effects of trichostatin A (TSA) on ceil proliferation and cell cycle in human gastric cancer cell line SGC-7901 in vitro and its mechanism. Methods SGC- 7901 cells were treated with 0.1, 0.5 and 2.0 μmol/L of TSA for 24 hrs. Growth inhibition rates of cells were measured by MTT assay and cell cycles were detected by flow cytometery (FCM). Expressions of eyclin D1 and p21 mRNA were measured by real-time PCR. Results The proliferations of SGC-7901 cells were inhibited when treated with TSA for 24 hrs. The inhibition rates in groups treat with 0.1, 0.5 or 2.0 μmol/L of TSA were 3.52%±6. 11%, 13.29%±4. 13% or 14.24%±2.80% ,respectively. The cell percentage of G0/G1 phase were higher in 0. 5 μmol/L group (71.26% ± 0.51%) and 2. 0 μmol/L group (71. 03%±0. 12%) compared with control group (51.12% ± 1.17%). The cell percentage of S phase were lower in 0.5 μmol/L group (13.55% ±0.44% ) and 2.0 μmol/L group (10. 63% ± 0. 63%) compared with control group (34. 60%±0.60%). The expression of cyclin D1 mRNA was down-regulated, whereas p21 mRNA expression was up-regulated. Conclusions TSA inhibits SCG-7901 gastric cancer cell proliferation by affecting the cell cycle control gene cyclin D1 and p21 mRNA expressions, which induce G0/G1 cell phase cycle arrest and ultimately impact on the growth of tumor cells.
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