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塞来昔布抑制鼻咽癌细胞增殖的分子机制研究

发布时间:2019-03-20 11:35
【摘要】:目的:研究塞来昔布对鼻咽癌细胞增殖、凋亡和细胞周期分布影响。 方法:通过MTT比色法检测不同药物浓度(5,10,25,50或75μmol/L)塞来昔布在作用鼻咽癌细胞HNE1和CNE1-LMP148h后对细胞增殖的影响。流式细胞术检测不同浓度塞来昔布(10,25,50或75μmol/L)作用鼻咽癌细胞HNE1和CNE1-LMP148h后细胞凋亡和细胞周期分布情况。 结果:MTT结果显示不同浓度塞来昔布可以抑制鼻咽癌细胞HNE1和CNE1-LMP1细胞增殖,呈浓度依赖性。流式细胞术结果显示(25,50μmol/L)塞来昔布可以诱导HNE1细胞凋亡和G0/G1期细胞周期阻滞,(50,75μmol/L)塞来昔布可以诱导CNE1-LMP1细胞凋亡,(25,50,75μmol/L)塞来昔布可以诱导CNE1-LMP1细胞G0/G1期细胞周期阻滞。 结论:塞来昔布可以抑制鼻咽癌HNE1和CNE1-LMP1细胞增殖,并诱导肿瘤细胞凋亡和G0/G1期细胞周期阻滞 目的:研究塞来昔布对鼻咽癌细胞IL-6/STAT3信号通路影响。 方法:用不同浓度的塞来昔布(0,10,25,50或75μmol/L)处理鼻咽癌HNE1和CNE1-LMP1细胞48h后采用WesternBlot检测细胞STAT3、pSTAT3y705、Survivin,Mcl-1,Bcl-2和CyclinD1蛋白表达。并采用WesternBlot检测塞来昔布是否可以抑制外源性IL-6诱导的STAT3磷酸化。 结果:在10,25,50μmol/L塞来昔布处理HNE1细胞后磷酸化的STAT3y705(pSTAT3y705)表达明显下降,Survivin,Mcl-1,Bcl-2和CyclinD1蛋白表达也随之表达下降。此外,在25,50,75μmol/L塞来昔布处理CNE1-LMP1细胞后磷酸化的STAT3y705(pSTAT3y705)表达明显下调,Survivin,Mcl-1,,Bcl-2和CyclinD1蛋白表达也随之下调。塞来昔布还可以抑制外源性IL-6诱导的STAT3磷酸化。 结论:塞来昔布可以抑制STAT3y705磷酸化,进而下调Survivin,Mcl-1,Bcl-2和CyclinD1蛋白表达。 目的:研究塞来昔布对鼻咽癌细胞AKT磷酸化影响。 方法:采用WesternBlot检测不同浓度的塞来昔布(10,25,50或75μmol/L)处理鼻咽癌HNE1、CNE1-LMP1和HONE1细胞48h后AKT磷酸化蛋白表达。 结果:WesternBlot结果显示塞来昔布可以抑制鼻咽癌细胞HNE1、CNE1-LMP1和HONE1细胞AKT磷酸化蛋白表达。 结论:塞来昔布可以抑制鼻咽癌细胞AKT磷酸化。
[Abstract]:Aim: to study the effects of celecoxib on proliferation, apoptosis and cell cycle distribution of nasopharyngeal carcinoma (NPC) cells. Methods: the effects of celecoxib (5 渭 mol / L, 10 渭 mol / L, 25 渭 mol / L, 50 渭 mol / L or 75 渭 mol / L) on the proliferation of nasopharyngeal carcinoma cell line HNE1 and CNE1-LMP148h were detected by MTT colorimetry. Apoptosis and cell cycle distribution of nasopharyngeal carcinoma cells (HNE1 and CNE1-LMP148h) treated with celecoxib (10,25,50 or 75 渭 mol / L) at different concentrations were detected by flow cytometry. Results: MTT results showed that different concentrations of celecoxib inhibited the proliferation of nasopharyngeal carcinoma cell line HNE1 and CNE1-LMP1 in a concentration-dependent manner. The results of flow cytometry showed that celecoxib (25,50 渭 mol / L) induced apoptosis and cell cycle arrest in G0/G1 phase of HNE1 cells, and (50,75 渭 mol / L) celecoxib induced apoptosis of CNE1-LMP1 cells. Celecoxib (25,50,75 渭 mol / L) induced cell cycle arrest in G0/G1 phase of CNE1-LMP1 cells. Conclusion: celecoxib can inhibit the proliferation of HNE1 and CNE1-LMP1 cells and induce apoptosis and cell cycle arrest in G0/G1 phase. Objective: to study the effect of celecoxib on IL-6/STAT3 signaling pathway of nasopharyngeal carcinoma cells. Methods: nasopharyngeal carcinoma HNE1 and CNE1-LMP1 cells were treated with different concentrations of celecoxib (0,10,25,50 or 75 渭 mol / L) for 48 hours and the expression of STAT3,pSTAT3y705,Survivin,Mcl-1,Bcl-2 and CyclinD1 protein was detected by WesternBlot. WesternBlot was used to detect whether celecoxib could inhibit exogenous IL-6-induced phosphorylation of STAT3. Results: after 10, 25, 50 渭 mol / L celecoxib treatment, the expression of phosphorylated STAT3y705 (pSTAT3y705), Survivin,Mcl-1,Bcl-2 and CyclinD1 protein decreased significantly in HNE1 cells. In addition, the expression of phosphorylated STAT3y705 (pSTAT3y705) and the expression of Survivin,Mcl-1,Bcl-2 and CyclinD1 proteins were down-regulated in CNE1-LMP1 cells treated with celecoxib at 25,50,75 渭 mol / L, respectively. Celecoxib also inhibited exogenous IL-6-induced phosphorylation of STAT3. Conclusion: celecoxib can inhibit the phosphorylation of STAT3y705 and down-regulate the expression of Survivin,Mcl-1,Bcl-2 and CyclinD1 proteins. Aim: to study the effect of celecoxib on phosphorylation of AKT in nasopharyngeal carcinoma cells. Methods: the expression of AKT phosphorylated protein in nasopharyngeal carcinoma (NPC) HNE1,CNE1-LMP1 and HONE1 cells treated with different concentrations of celecoxib (10,25,50 or 75 渭 mol / L) for 48 h was detected by WesternBlot. Results: WesternBlot results showed that celecoxib inhibited the expression of AKT phosphorylation protein in nasopharyngeal carcinoma cells HNE1,CNE1-LMP1 and HONE1 cells. Conclusion: celecoxib can inhibit the phosphorylation of AKT in nasopharyngeal carcinoma cells.
【学位授予单位】:华中科技大学
【学位级别】:博士
【学位授予年份】:2013
【分类号】:R739.63

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相关期刊论文 前7条

1 吴仁瑞;吴少雄;赵充;谢方云;高剑铭;胡伟汉;高远红;李凤岩;崔甜甜;卢泰祥;;h-R3联合放疗治疗局部晚期鼻咽癌的Ⅱ期临床研究[J];癌症;2007年08期

2 何本夫;孙爱民;黄碧燕;王雯s

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