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作 者:冷洁[1] 田甜[1] 赵晶[2] 高向阳[2] 宋超[2] 高超[2]
机构地区:[1]徐州医学院研究生学院,江苏徐州221004 [2]徐州医学院附属医院肿瘤科,江苏徐州221002
出 处:《徐州医学院学报》2016年第2期93-97,共5页Acta Academiae Medicinae Xuzhou
摘 要:目的研究非甾体抗炎药戊地昔布(valdecoxib)对人直肠癌Col0320细胞迁移及侵袭能力的影响,并初步探讨其可能的机制。方法用不同浓度(0、50、100、200μmol/L)的戊地昔布分别处理Col0320细胞24h。采用划痕及TransweU小室实验检测细胞迁移及侵袭能力的变化;采用Westernblot实验检测戊地昔布作用于Col0320细胞后细胞内环氧化酶-2(COX-2)蛋白的表达变化,并检测与迁移、侵袭相关的基质金属蛋白酶-2(MMP-2)及钙黏附蛋白-E(E—ceherin)的表达变化。结果不同浓度的戊地昔布分别作用于Col0320细胞24h后,50、100及200μmol/L戊地昔布处理组细胞的迁移率较对照组明显下降,与对照组相比差异具有统计学意义(F=399.1,P〈0.01);Transwell实验结果显示戊地昔布处理组侵袭细胞数较对照组明显减少,与对照组比较差异具有统计学意义(F=36.5,P〈0.01);Westernblot实验结果显示戊地昔布处理组相对于对照组细胞内COX-2蛋白表达量明显降低(F=52.04,P〈0.01),E—ceherin表达量增加(F=60.3,P〈0.01),MMP-2蛋白表达量减少(F=100.3,P〈0.01)。结论戊地昔布可以抑制直肠癌Col0320细胞的迁移及侵袭能力,其机制可能是通过抑制COX-2的表达实现的。此外,还可能是通过调节与EMT相关的MMP-2及E—caherin蛋白的表达而实现的。Objective To discusses the effects of valdecoxib on the migration and invasion of human colorectal cancer Colo320 cells and possible mechanisms involved. Methods Colo320 cells were exposed to different concentra- tions of valdecoxib (0, 50, 100, and 200 tool/L) for 24 h. Then, the effects of valdecoxib on the migration and inva- sion/metastasis of Colo320 cells were determined by wound healing assay and Transwell method. The levels of COX - 2, MMP - 2 and E - cadherin in Colo320 ceils were measured by Western blotting. Results Exposure to 50, 100 and 200 mol/L of valdecoxib could obviously inhibit the migration of Colo320 cells, compared with the control ( F = 399. 1, P 〈 0.01 ). According to Transwell assay results, the number of invasive cells were remarkably lower in the valdecoxib treat- ment group than that in the control ( F = 36. 5, P 〈 0.01 ). Compared with the control, the valdecoxib treatment group produced markedly decreased levels of COX - 2 ( F = 52.04, P 〈 0.01 ) and MMP - 2 ( F = 100. 3, P 〈 0.01 ), but in- creased amounts of E - cadherin ( F = 60. 3, P 〈 0.01 ). Conclusion Valdecoxib can inhibit the migration and invasion of Colo320 cells, which may be associated with inhibition of COX - 2 and MMP - 2 expression and up - regulation of E - cadhefin protein.
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