FDI-6對(duì)喉癌細(xì)胞惡性生物學(xué)行為的影響及其機(jī)制
發(fā)布時(shí)間:2018-06-23 23:23
本文選題:叉頭結(jié)構(gòu)域抑制物(FDI-6) + 叉頭盒M1(FoxM1) ; 參考:《重慶醫(yī)科大學(xué)》2017年碩士論文
【摘要】:目的:探討新型小分子抑制劑叉頭結(jié)構(gòu)域抑制物FDI-6(Forkhead Domain Inhibitory-6,FDI-6)對(duì)喉癌Hep-2細(xì)胞增殖、凋亡、侵襲和遷移的影響及其可能機(jī)制。方法:采用MTT法檢測(cè)不同濃度(5~80)μmol/L FDI-6處理12 h、24 h后,Hep-2細(xì)胞的增殖情況。采用流式細(xì)胞術(shù)(flow cytometry,FCM)檢測(cè)(10、20)μmol/L FDI-6處理Hep-2細(xì)胞24h后細(xì)胞凋亡情況、Transwell小室法檢測(cè)細(xì)胞侵襲及遷移能力的變化。實(shí)時(shí)熒光定量PCR(Quantitative Real-time PCR,qRT-PCR)檢測(cè)叉頭盒M1(FoxM1)的mRNA水平、蛋白質(zhì)免疫印記法檢測(cè)FoxM1、Bcl-2、Bax的蛋白表達(dá)水平。結(jié)果:FDI-6可抑制喉癌Hep-2細(xì)胞的增殖,其抑制作用呈濃度和時(shí)間依賴性(P值均0.05)。與DMSO對(duì)照組相比,FDI-6處理組細(xì)胞凋亡率明顯上升,細(xì)胞的侵襲、遷移能力明顯受抑,且濃度越大,抑制作用越明顯(P0.05)。FDI-6處理喉癌Hep-2細(xì)胞24 h后FoxM1mRNA和蛋白水平無(wú)明顯改變(p0.05)。Bcl-2蛋白表達(dá)下降,Bax蛋白表達(dá)升高(p0.05),而在細(xì)胞核中FoxM1的蛋白水平隨FDI-6濃度升高而降低(p0.05)。結(jié)論:FDI-6可抑制喉癌細(xì)胞Hep-2的增殖、侵襲、遷移,并誘導(dǎo)細(xì)胞凋亡,可能與下調(diào)細(xì)胞核中FoxM1及誘導(dǎo)腫瘤細(xì)胞凋亡相關(guān)。
[Abstract]:Aim: to investigate the effects of a novel small molecular inhibitor, forkhead domain inhibitor FDI-6 (FDI-6), on the proliferation, apoptosis, invasion and migration of laryngeal cancer cell line Hep-2 and its possible mechanism. Methods: MTT assay was used to detect the proliferation of Hep-2 cells treated with different concentrations of (5o 80) 渭 mol / L FDI-6 for 12 h or 24 h. The apoptosis of Hep-2 cells was detected by flow cytometry (10 ~ 20 渭 mol / L FDI-6) for 24 hours. The mRNA level of forkhead box M1 (FoxM1) was detected by quantitative real-time PCR and the protein expression level of FoxM1Bcl-2mBax was detected by protein imprinting. Results the proliferation of Hep-2 cells was inhibited by 1% FDI-6 in a concentration and time dependent manner (P < 0.05). Compared with the DMSO control group, the apoptosis rate of the treated group was significantly increased, the invasion and migration ability of the cells were inhibited obviously, and the higher the concentration was, the higher the cell apoptosis rate was. The inhibitory effect was more obvious (P0.05). FDI-6 had no obvious changes in FoxM1 mRNA and protein levels (p0.05) .Bcl-2 protein expression decreased (p0.05), but FoxM1 protein level decreased with the increase of FDI-6 concentration (p0.05). Conclusion the cell proliferation invasion migration and apoptosis of laryngeal carcinoma cell line Hep-2 can be inhibited by WFDI-6 which may be related to the down-regulation of FoxM1 in the nucleus and the induction of apoptosis in tumor cells.
【學(xué)位授予單位】:重慶醫(yī)科大學(xué)
【學(xué)位級(jí)別】:碩士
【學(xué)位授予年份】:2017
【分類號(hào)】:R739.65
【參考文獻(xiàn)】
相關(guān)期刊論文 前3條
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