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CUG连接蛋白1基因在前列腺癌的表达及其功能研究 被引量:3

Expression and function of CUG-binding protein 1 gene in prostate carcinoma
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摘要 目的:探讨CUG连接蛋白1(CUG-Binding Protein 1,CUGBP1)基因在前列腺癌的表达及其蛋白功能。方法:用定量RT-PCR法在前列腺癌组织和癌旁组织中检测CUGBP的mRNA水平。Western blot法检测4种前列腺癌细胞株(22RV1,PC-3,DU145,LNCaP clone FGC)中CUGBP1的表达。利用RNA干扰技术检测PC-3细胞在CUGBP1基因沉默后细胞的增殖与凋亡状态。利用定量RT-PCR法确定其下游调控基因的mRNA水平。结果:CUGBP1在PC-3和22RV1细胞株中高表达。CUGBP1的mRNA在前列腺癌组织中较癌旁组织显著增高。CUGBP1基因shRNA导致CUGBP1基因沉默后抑制了PC-3细胞株的增殖并诱导其凋亡;同时,使前列腺癌细胞在细胞周期上发生G1期阻滞。CUGBP1基因被干扰以后,PC-3细胞株中CDKN1A的mRNA水平发生明显上调,同时BCL2、PCNA、MCM2和MCM3基因的mRNA水平发生明显下调。结论:CUGBP1基因和前列腺癌相关。CUGBP1基因可能通过上调/下调下游基因来调节前列腺癌细胞的凋亡,改变细胞的增殖和细胞周期。 Objective:To study on the expression and function of CUG-binding protein 1(CUGBP1) in prostate carcinoma.Methods: The CUGBP1mRNA levels in the prostate carcinoma specimen and the adjacent non-carcinoma tissues were detected by quantitative RT-PCR.The expressions of four kinds prostate carcinoma cell strains(22RV1,PC-3,DU145,LNCaP clone FGC) in CUGBP1 were detected by Western blot.The proliferation and apoptosis of cell line PC-3 after silencing CUGBP1 were examed by RNA interference technique.The mRNA levels of downstream related genes in cell line PC-3 were determined by quantitative RT-PCR.Results:CUGBP1 was highly expressed in PC-3 and 22RV1.The CUGBP1 mRNA level in prostate carcinoma tissues was higher than that in adjacent non-carcinoma tissues.The CUGBP1 gene silencing,which was induced by shRNA lentivirus,suppressed the proliferation and apoptosis of cell line PC-3 and increased the proportion of cells in G1 phase.The mRNA level of CDKN1A in PC-3 cell line was up-regulated while that of BCL2,PCNA,MCM2 and MCM3 was down-regulated after CUGBP1 gene silencing.Conclusion:CUGBP1 gene may regulate the apoptosis,proliferation and cell cycle of prostate carcinoma cells through up-regulating and down-regulating downstream genes.
出处 《重庆医科大学学报》 CAS CSCD 北大核心 2012年第6期539-543,共5页 Journal of Chongqing Medical University
关键词 前列腺癌 CUG连接蛋白1基因 增殖 凋亡 prostate cancer CUG-binding protein 1 gene proliferation apoptosis
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