KLF5转录因子抑制TRAIL诱导PC-3前列腺癌细胞凋亡的分子机制  

KLF5 suppresses TRAIL-induced cell apoptosis in PC-3 prostate cancer cells

作　　者：杨超 石琦 马建斌 郭鹏[1] 贺大林[1] YANG Chao;SHI Qi;MA Jian-bin;GUO Peng;HE Da-lin(Department of Urology,The First Affiliated Hospital of Xi'an Jiaotong University,Xi'an 710061,China)

机构地区：[1]西安交通大学第一附属医院泌尿外科

出　　处：《西安交通大学学报（医学版）》2020年第2期206-209,共4页Journal of Xi’an Jiaotong University（Medical Sciences）

基　　金：国家自然科学基金资助项目(No.81672557,81672958)~~

摘　　要：目的探究通过抑制KLF5表达促进TRAIL诱导的前列腺癌PC-3细胞凋亡的分子机制。方法在TRAIL诱导下,使用MTT实验、流式细胞实验、Western blot及qRT-PCR检测KLF5敲低组与对照组的PC-3细胞在细胞活性、凋亡比例及凋亡相关标志物的表达。结果在PC-3细胞中抑制KLF5表达后,TRAIL诱导下的细胞凋亡明显增加,TRAIL受体DR4、DR5表达上升,凋亡抑制因子c-FLIP蛋白表达下调,但是其mRNA表达水平不变。结论抑制KLF5,可以通过上调TRAIL受体、下调c-FLIP蛋白表达的途径,促进TRAIL诱导的前列腺癌PC-3细胞的凋亡,抑制肿瘤细胞增殖。使用小干扰RNA或小分子药物抑制KLF5表达,可能是潜在的激素非敏感前列腺癌治疗手段。Objective To explore the possibility of promoting tumor necrosis factor-related apoptosis inducing ligand(TRAIL)-induced apoptosis in prostate cancer PC-3 cell by inhibiting Krüppel-like factor 5(KLF5).Methods MTT assay,flow cytometry,Western blot assay and qRT-PCR assay were deployed to detect the cell viability,apoptosis and apoptotic markers in KLF5-inhibited and TRAIL-induced PC-3 cells.Results After KLF5 was inhibited in TRAIL-induced PC-3 cells,cell viability reduced,apoptosis enhanced,the expressions of DR4 and DR5 increased while the expression of cellular fas-associated death domain-like interleukin-1βconverting enzyme inhibitory protein(c-FLIP)decreased.Conclusion Inhibiting KLF5 suppresses cell viability by promoting TRAIL-induced apoptosis in prostate cancer cell PC-3.It may be a potential means to treat hormone-insensitive prostate cancer.

关 键 词：前列腺癌 Krüppel样因子5(KLF5) 肿瘤坏死因子相关凋亡诱导配体(TRAIL) 凋亡 细胞型Fas相关死亡域样白介素-1β转换酶抑制蛋白(c-FLIP) 

分 类 号：R737.14[医药卫生—肿瘤]