基于Sirt1/p53信号通路探究NK4基因对非霍奇金淋巴瘤细胞增殖和凋亡的机制研究  

The Mechanism of NK4 Gene on Proliferation and Apoptosis in Non-Hodgkin Lymphoma Cells Based on Sirt1/p53 Signaling Pathway

作　　者：贲海祥 徐娟[1] BEN Haixiang;XU Juan(Rugao People's Hospital,Jiangsu Nantong 226500,China)

机构地区：[1]江苏省如皋市人民医院血液科,江苏如皋226500

出　　处：《河北医学》2023年第8期1263-1267,共5页Hebei Medicine

基　　金：江苏省优势学科建设工程项目,(编号:YSHL0814-812)。

摘　　要：目的:本研究旨在探究NK4基因对非霍奇金淋巴瘤细胞增殖和凋亡的影响机制。方法:通过qRT-PCR检测NHL细胞系(Jurkat和Raji)及正常B细胞(normal)中NK4 mRNA表达水平,采取pcDNA3.1-NK4转染至Raji细胞中由此提高NK4表达水平。通过CCK-8检测细胞增殖,流式细胞术检测细胞凋亡,transwell迁移实验检测细胞迁移、侵袭能力以此评估细胞生长进展。采取western blot检测Sirt1/p53信号通路相关蛋白。结果:NK4基因在NHL细胞低表达,在NHL细胞株Raji细胞中上调NK4表达水平后,Raji细胞增殖、迁移和侵袭能力显著下降,而细胞凋亡率上升。此外,上调NK4表达水平使得Sirt1蛋白表达水平显著下降,p53水平显著上升。额外添加Sirt1激活剂SRT1720后细胞生长进展受到部分抑制。结论:NK4基因介导Sirt1/p53信号通路抑制非霍奇金淋巴瘤细胞增殖,促进其凋亡。Objective:To investigate the effect of NK4 gene on the proliferation and apoptosis of non-Hodgkin’s lymphoma cells.Methods:The expression levels of NK4 mRNA in NHL cell lines(Jurkat and Raji cells)and normal B cells(normal)were detected by qRT-PCR.pcDNA3.1-NK4 was transfected into Raji cells to increase the expression level of NK4.Cell proliferation was detected by CCK-8,apoptosis was detected by flow cytometry,and cell migration and invasion were detected by transwell assay to evaluate cell growth progress.Western blot was used to detect Sirt1/p53 signaling pathway-related proteins.Results:NK4 gene was lowly expressed in NHL cells.After up-regulating NK4 expression in NHL cell line Raji cells,the proliferation,migration and invasion ability of Raji cells decreased significantly,while the apoptosis rate increased.In addition,up-regulation of NK4 expression significantly decreased Sirt1 protein expression and increased p53 level.Addition of Sirt1 activator SRT1720 partially inhibited cell growth.Conclusion:NK4 gene mediated Sirt1/p53 signaling pathway inhibited proliferation and promoted apoptosis of non-Hodgkin lymphoma cells.

关 键 词：非霍奇金淋巴瘤 细胞增殖 细胞凋亡 

分 类 号：R733.1[医药卫生—肿瘤]