西妥昔單抗聯(lián)合紫杉醇對人鼻咽癌CNE-1細胞抑制作用及其分子機制研究
發(fā)布時間:2018-10-17 07:08
【摘要】:目的:本研究以人鼻咽癌CNE-1細胞為研究對象,探討西妥昔單抗(Cetuximab)聯(lián)合紫杉醇(Paclitaxel,PTX)對其增殖及凋亡的影響,并進一步研究其可能的分子機制。 方法:培養(yǎng)人鼻咽癌CNE-1細胞株,隨機將細胞分為空白對照組、紫杉醇組、西妥昔單抗組和聯(lián)合用藥組。用MTT法檢測細胞抑制率,流式細胞術(shù)檢測細胞凋亡率,實時熒光定量PCR (RT-PCR法)及Western-blot法檢測EGFR、MMP-2的mRNA和蛋白表達。 結(jié)果:聯(lián)合用藥組的細胞抑制率高于紫杉醇組和西妥昔單抗組(P值分別為0.002、0.000);聯(lián)合用藥組的細胞凋亡率高于紫杉醇組和西妥昔單抗組(P值均為0.000);聯(lián)合用藥組的EGFR、MMP-2的mRNA表達值均低于紫杉醇組和西妥昔單抗組(各組間EGFR mRNA的表達P值分別為0.000、0.001;MMP-2mRNA的表達P值均為0.000);聯(lián)合用藥組的EGFR、MMP-2的蛋白值表達均低于紫杉醇組和西妥昔單抗組(各組間EGFR蛋白的表達P值均為0.000;MMP-2蛋白的表達P值分別為為0.000、0.006)。 結(jié)論:西妥昔單抗聯(lián)合紫杉醇能夠抑制人鼻咽癌CNE-1細胞的增殖,,促進其凋亡,兩者聯(lián)用具有協(xié)同作用,其分子機制可能是通過抑制腫瘤細胞EGFR、MMP-2的表達來實現(xiàn)。
[Abstract]:Aim: to investigate the effects of cetuximab (Cetuximab) combined with paclitaxel (Paclitaxel,PTX) on the proliferation and apoptosis of human nasopharyngeal carcinoma (NPC) CNE-1 cells and to further study its molecular mechanism. Methods: human nasopharyngeal carcinoma (NPC) CNE-1 cell lines were cultured and randomly divided into three groups: blank control group, paclitaxel group, cetuximab group and combination therapy group. Cell inhibition rate was detected by MTT assay, apoptosis rate was detected by flow cytometry, mRNA and protein expression of EGFR,MMP-2 were detected by real-time fluorescence quantitative PCR (RT-PCR) and Western-blot assay. Results: the cell inhibition rate in combination group was higher than that in paclitaxel group and cetuximab group (P = 0.002 + 0.000), the apoptosis rate in combination group was higher than that in paclitaxel group and cetuximab group (P = 0.000). The mRNA expression of EGFR,MMP-2 in combination group was lower than that in paclitaxel group and cetuximab group (P = 0.0000.0001MP-2, P = 0.000). The expression of EGFR,MMP-2 protein in combination group was lower than that in paclitaxel group and cetuximab group (P value of 0.000mmp2protein was 0.000,0.006, respectively). Conclusion: cetuximab combined with paclitaxel can inhibit the proliferation and promote the apoptosis of human nasopharyngeal carcinoma (NPC) CNE-1 cells. The molecular mechanism of the combination of cetuximab and paclitaxel may be by inhibiting the expression of EGFR,MMP-2 in human nasopharyngeal carcinoma cells.
【學(xué)位授予單位】:重慶醫(yī)科大學(xué)
【學(xué)位級別】:碩士
【學(xué)位授予年份】:2014
【分類號】:R734.2
本文編號:2275920
[Abstract]:Aim: to investigate the effects of cetuximab (Cetuximab) combined with paclitaxel (Paclitaxel,PTX) on the proliferation and apoptosis of human nasopharyngeal carcinoma (NPC) CNE-1 cells and to further study its molecular mechanism. Methods: human nasopharyngeal carcinoma (NPC) CNE-1 cell lines were cultured and randomly divided into three groups: blank control group, paclitaxel group, cetuximab group and combination therapy group. Cell inhibition rate was detected by MTT assay, apoptosis rate was detected by flow cytometry, mRNA and protein expression of EGFR,MMP-2 were detected by real-time fluorescence quantitative PCR (RT-PCR) and Western-blot assay. Results: the cell inhibition rate in combination group was higher than that in paclitaxel group and cetuximab group (P = 0.002 + 0.000), the apoptosis rate in combination group was higher than that in paclitaxel group and cetuximab group (P = 0.000). The mRNA expression of EGFR,MMP-2 in combination group was lower than that in paclitaxel group and cetuximab group (P = 0.0000.0001MP-2, P = 0.000). The expression of EGFR,MMP-2 protein in combination group was lower than that in paclitaxel group and cetuximab group (P value of 0.000mmp2protein was 0.000,0.006, respectively). Conclusion: cetuximab combined with paclitaxel can inhibit the proliferation and promote the apoptosis of human nasopharyngeal carcinoma (NPC) CNE-1 cells. The molecular mechanism of the combination of cetuximab and paclitaxel may be by inhibiting the expression of EGFR,MMP-2 in human nasopharyngeal carcinoma cells.
【學(xué)位授予單位】:重慶醫(yī)科大學(xué)
【學(xué)位級別】:碩士
【學(xué)位授予年份】:2014
【分類號】:R734.2
【參考文獻】
相關(guān)期刊論文 前1條
1 ;索拉非尼治療晚期及轉(zhuǎn)移性頭頸部鱗癌的臨床Ⅱ期研究評價[J];中國口腔頜面外科雜志;2010年05期
本文編號:2275920
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