TTK在鼻咽癌组织中的表达及其对鼻咽癌细胞生物学行为的影响  

Expression of TTK in NPC tissues and its influence on the biological behavior of NPC cells

作　　者：吴蕴生 李萍 冯燚源 王安生 张文思 赵海琪 张雄 杨洪斌[2] WU Yunsheng;LI Ping;FENG Yiyuan;WANG Ansheng;ZHANG Wensi;ZHAO Haiqi;ZHANG Xiong;YANG Hongbin(North Sichuan Medical College,Sichuan Nanchong 637000,China;Department of Otorhinolaryngology Head and Neck Surgery,Affiliated Hospital of North Sichuan Medical College,Sichuan Nanchong 637000,China)

机构地区：[1]川北医学院,四川南充637000 [2]川北医学院附属医院耳鼻咽喉头颈外科,四川南充637000

出　　处：《现代肿瘤医学》2023年第21期3945-3950,共6页Journal of Modern Oncology

基　　金：川北医学院附属医院课题基金(编号:2022JC016)。

摘　　要：目的:运用生物信息学方法筛选出鼻咽癌相关核心基因苏氨酸和酪氨酸激酶(threonine and tyrosine kinase,TTK),探讨其在鼻咽癌组织中的表达;敲低TTK对人鼻咽癌CNE2细胞生物学行为的影响及可能存在的机制。方法:利用生物信息学方法,基于GEO数据库中鼻咽癌患者数据集,筛选出与鼻咽癌发生发展相关核心基因TTK;免疫组化实验检测TTK在鼻咽癌组织和慢性鼻咽炎组织中的表达;慢病毒转染人鼻咽癌CNE2细胞敲低TTK后,CCK-8实验检测敲低TTK对CNE2细胞增殖的影响;流式细胞实验检测TTK低表达后对CNE2细胞凋亡及周期的影响;Western Blot实验检测CNE2细胞在TTK低表达时,凋亡信号通路中关键蛋白BCL-2、BAX蛋白表达情况,探究TTK在鼻咽癌发生发展中可能存在的机制。结果:生物信息学方法筛选出核心基因TTK。TTK在鼻咽癌组织中呈现高表达,在慢性鼻咽炎组织中呈现低表达。敲低TTK后,CNE2细胞增殖受到抑制,细胞凋亡增加。细胞周期G_(1)期减少且S期和G_(2)期增加,提示敲低TTK导致细胞阻滞于S/G_(2)期。TTK的沉默导致CNE2细胞中BCL-2蛋白表达下降,BAX蛋白表达升高。结论:TTK在鼻咽癌组织中高表达。敲低TTK影响鼻咽癌CNE2细胞的增殖、凋亡、周期和凋亡通路关键蛋白BCL-2、BAX的表达,表明TTK可能通过凋亡通路参与鼻咽癌的发生发展。Objective:The threonine and tyrosine kinase(TTK) was selected to determine its expression in nasopharyngeal carcinoma(NPC) tissues and the effects of TTK knockdown and the biological mechanism of human NPC CNE2 cells.Methods:Using a bioinformatics approach,based on the NPC patient dataset in the GEO database,TTK,the core gene associated with the development of nasopharyngeal carcinoma was screened.Immunohistochemical experiments of TTK expression in NPC tissues and chronic NPC tissues.After the knockdown of TTK by lentiviral transfection of human NPC CNE2 cells,the effect of TTK knockdown on the proliferation of CNE2 cells was tested by CCK-8 experiment.The effect of low TTK expression on apoptosis and cycle of CNE2 cells was tested in flow cell experiments.Western Blot was used to detect the expression of BCL-2 and BAX,the key protein in the apoptosis signaling pathway,in CNE2 cells with low expression of TTK.To explore the possible mechanism of TTK in the development of NPC.Results:The core gene TTK was selected by bioinformatics methods.TTK showed high expression in NPC tissues and low expression in chronic NPC tissues.After TTK knockdown,CNE2 cell proliferation was inhibited and cell apoptosis was increased.Reduced G_(1) phase of the cell cycle and increased S and G_(2) phases,suggesting that TTK knockdown caused cell arrest in the S/G_2phase.Silencing of TTK led to a decrease in BCL-2 protein expression and an elevated BAX protein expression in CNE2 cells.Conclusion:TTK is highly expressed in NPC tissues.TTK knockdown affected the expression of BCL-2 and BAX of proliferation,apoptosis,cycle and apoptotic pathway in NPC CNE2 cells,indicating that TTK may participate in the development and development of NPC through the apoptotic pathway.

关 键 词：鼻咽癌 TTK 生物信息学 免疫组化 增殖 凋亡 细胞周期 凋亡通路 

分 类 号：R739.6[医药卫生—肿瘤]