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塞來昔布抑制鼻咽癌細胞增殖的分子機制研究

發(fā)布時間:2019-03-20 11:35
【摘要】:目的:研究塞來昔布對鼻咽癌細胞增殖、凋亡和細胞周期分布影響。 方法:通過MTT比色法檢測不同藥物濃度(5,10,25,50或75μmol/L)塞來昔布在作用鼻咽癌細胞HNE1和CNE1-LMP148h后對細胞增殖的影響。流式細胞術檢測不同濃度塞來昔布(10,25,50或75μmol/L)作用鼻咽癌細胞HNE1和CNE1-LMP148h后細胞凋亡和細胞周期分布情況。 結果:MTT結果顯示不同濃度塞來昔布可以抑制鼻咽癌細胞HNE1和CNE1-LMP1細胞增殖,呈濃度依賴性。流式細胞術結果顯示(25,50μmol/L)塞來昔布可以誘導HNE1細胞凋亡和G0/G1期細胞周期阻滯,(50,75μmol/L)塞來昔布可以誘導CNE1-LMP1細胞凋亡,(25,50,75μmol/L)塞來昔布可以誘導CNE1-LMP1細胞G0/G1期細胞周期阻滯。 結論:塞來昔布可以抑制鼻咽癌HNE1和CNE1-LMP1細胞增殖,并誘導腫瘤細胞凋亡和G0/G1期細胞周期阻滯 目的:研究塞來昔布對鼻咽癌細胞IL-6/STAT3信號通路影響。 方法:用不同濃度的塞來昔布(0,10,25,50或75μmol/L)處理鼻咽癌HNE1和CNE1-LMP1細胞48h后采用WesternBlot檢測細胞STAT3、pSTAT3y705、Survivin,Mcl-1,Bcl-2和CyclinD1蛋白表達。并采用WesternBlot檢測塞來昔布是否可以抑制外源性IL-6誘導的STAT3磷酸化。 結果:在10,25,50μmol/L塞來昔布處理HNE1細胞后磷酸化的STAT3y705(pSTAT3y705)表達明顯下降,Survivin,Mcl-1,Bcl-2和CyclinD1蛋白表達也隨之表達下降。此外,在25,50,75μmol/L塞來昔布處理CNE1-LMP1細胞后磷酸化的STAT3y705(pSTAT3y705)表達明顯下調,Survivin,Mcl-1,,Bcl-2和CyclinD1蛋白表達也隨之下調。塞來昔布還可以抑制外源性IL-6誘導的STAT3磷酸化。 結論:塞來昔布可以抑制STAT3y705磷酸化,進而下調Survivin,Mcl-1,Bcl-2和CyclinD1蛋白表達。 目的:研究塞來昔布對鼻咽癌細胞AKT磷酸化影響。 方法:采用WesternBlot檢測不同濃度的塞來昔布(10,25,50或75μmol/L)處理鼻咽癌HNE1、CNE1-LMP1和HONE1細胞48h后AKT磷酸化蛋白表達。 結果:WesternBlot結果顯示塞來昔布可以抑制鼻咽癌細胞HNE1、CNE1-LMP1和HONE1細胞AKT磷酸化蛋白表達。 結論:塞來昔布可以抑制鼻咽癌細胞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.
【學位授予單位】:華中科技大學
【學位級別】:博士
【學位授予年份】:2013
【分類號】:R739.63

【參考文獻】

相關期刊論文 前7條

1 吳仁瑞;吳少雄;趙充;謝方云;高劍銘;胡偉漢;高遠紅;李鳳巖;崔甜甜;盧泰祥;;h-R3聯(lián)合放療治療局部晚期鼻咽癌的Ⅱ期臨床研究[J];癌癥;2007年08期

2 何本夫;孫愛民;黃碧燕;王雯s

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