香烟烟雾促进膀胱癌干细胞的自我更新和干性基因的表达
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摘要
目的:探讨香烟烟雾对膀胱癌干细胞自我更新能力和干性基因表达的影响。方法:用不同浓度(0%、0. 1%和0. 25%)的香烟烟雾悬液处理人膀胱癌细胞UM-UC-3来源的膀胱癌干细胞4 d,显微镜下观察膀胱癌干细胞球大小及数量,蛋白质印迹检测干性基因CD44、ALDH1-A1、OCT-4、Nanog等的蛋白表达。结果:0. 1%和0. 25%的香烟烟雾悬液能够促进膀胱癌干细胞细胞球的形成,香烟烟雾处理组的细胞球明显大于对照组;蛋白质印迹结果显示,0. 1%和0. 25%的香烟烟雾悬液处理的膀胱癌干细胞CD44、ALDH1-A1、OCT-4、Nanog表达显著增加。结论:香烟烟雾能够促进膀胱癌干细胞的自我更新和干性基因的表达。
Objective: To investigate the effect of tobacco smoke on self-renewal ability and stemness genes expression of bladder cancer stem cells. Methods: The bladder cancer stem cells obtained from human bladder cancer cells UM-UC-3 were treated with different concentrations of cigarette smoke extract(CSE,0%,0. 1% and 0. 25%) for 4 days. The effect of CSE on the sizes and quantities of bladder cancer stem cells spheres were observed. The expression of stemness genes CD44,ALDH1-A1 OCT-4,and Nanog were detected by Western blotting. Results: 0. 1% and 0. 25% CSE promoted the formation of bladder cancer stem cell spheres,while the cell spheres of CSE groups were significantly larger than the control group; Western blotting results showed that the expression of CD44,ALDH1-A1,OCT-4,and Nanog were significantly increased in 0. 1% and 0. 25% CSE groups. Conclusion: Tobacco smoke can promote the self-renewal ability of bladder cancer stem cells and upregulate the expression levels of CD44,ALDH1-A1 OCT-4,and Nanog.
Objective: To investigate the effect of tobacco smoke on self-renewal ability and stemness genes expression of bladder cancer stem cells. Methods: The bladder cancer stem cells obtained from human bladder cancer cells UM-UC-3 were treated with different concentrations of cigarette smoke extract(CSE,0%,0. 1% and 0. 25%) for 4 days. The effect of CSE on the sizes and quantities of bladder cancer stem cells spheres were observed. The expression of stemness genes CD44,ALDH1-A1 OCT-4,and Nanog were detected by Western blotting. Results: 0. 1% and 0. 25% CSE promoted the formation of bladder cancer stem cell spheres,while the cell spheres of CSE groups were significantly larger than the control group; Western blotting results showed that the expression of CD44,ALDH1-A1,OCT-4,and Nanog were significantly increased in 0. 1% and 0. 25% CSE groups. Conclusion: Tobacco smoke can promote the self-renewal ability of bladder cancer stem cells and upregulate the expression levels of CD44,ALDH1-A1 OCT-4,and Nanog.
引文
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[2]Leta2iováS,Medve'ováA,ovcˇíkováA,et al.Bladder cancer,a review of the environmental risk factors[J].Environ Health,2012,11(Suppl 1):S11.
[3]Chen L,Nergard J,Ni L,et al.Long-term exposure to cigarette smoke extract induces hypomethylation at the RUNX3 and IGF2-H19 loci in immortalized human urothelial cells[J].PLo S One,2013,8:e65513.
[4]Liang Z,Xie W,Wu R,et al.Inhibition of tobacco smoke-induced bladder MAPK activation and epithelialmesenchymal transition in mice by curcumin[J].Int JClin Exp Pathol,2015,8(5):4503-4513.
[5]Geng H,Zhao L,Liang Z,et al.ERK5 positively regulates cigarette smoke-induced urocystic epithelial-mesenchymal transition in SV-40 immortalized human urothelial cells[J].Oncol Rep,2015,34(3):1581-1588.
[6]Cumberbatch MGK,Noon AP.Epidemiology,aetiology and screening of bladder cancer[J].Transl Androl Urol,2019,8(1):5-11.
[7]Kallifatidis G,Smith DK,Morera DS,et al.β-Arrestins regulate stem cell-like phenotype and response to chemotherapy in bladder cancer[J].Mol Cancer Ther,2019,18(4):801-811.
[8]Wang J,Chen J,Jiang Y,et al.Wnt/β-catenin modulates chronic tobacco smoke exposure-induced acquisition of pulmonary cancer stem cell properties and diallyl trisulfide intervention[J].Toxicol Lett,2018,291:70-76.
[9]Xie C,Zhu J,Wang X,et al.Tobacco smoke induced hepatic cancer stem cell-like properties through IL-33/p38 pathway[J].J Exp Clin Cancer Res,2019,38(1):39.
[10]Qian W,Kong X,Zhang T,et al.Cigarette smoke stimulates the stemness of renal cancer stem cells via Sonic Hedgehog pathway[J].Oncogenesis,2018,7(3):24.