目的探讨弥漫大B细胞淋巴瘤(DLBCL)中miR-125a-5p的表达水平及与临床病理特征、预后和NF-κB/p65、Bcl2、Caspase3、Ki-67蛋白表达的关系。方法收集84例DLBCL病例,以同期10例淋巴结反应性增生组织作为对照,采用SYBR Green real-time逆...目的探讨弥漫大B细胞淋巴瘤(DLBCL)中miR-125a-5p的表达水平及与临床病理特征、预后和NF-κB/p65、Bcl2、Caspase3、Ki-67蛋白表达的关系。方法收集84例DLBCL病例,以同期10例淋巴结反应性增生组织作为对照,采用SYBR Green real-time逆转录聚合酶链反应(real-time RT-PCR)检测其miR-125a-5p的表达水平,免疫组化检测NF-κB/p65、Bcl2、Caspase3、Ki-67蛋白表达,收集临床病理资料并随访,结合患者临床资料及预后进行统计学分析。结果在DLBCL样本中miR-125a-5p表达量上调,其表达量是淋巴结反应性增生的(4.99±8.22)倍(P=0.002);miR-125a-5p在DLBCL中的上调与Hans分型non-GCB亚型存在相关性(P=0.027);miR-125a-5p在DLBCL中的上调表达与NF-κB/p65、Bcl2、Caspase3蛋白表达存在显著相关性(P值分别为0.031、0.030、0.022);在DLBCL中Hans分型non-GCB亚型与NF-κB/p65蛋白具有显著相关性(P=0.002);Kaplan-Meier生存分析显示,miR-125a-5p的高表达与DLBCL患者预后有关(P=0.038);多因素Cox分析显示,miR-125a-5p的高表达可能是DLBCL患者预后的独立危险因素(P=0.013)。结论 miR-125a-5p可能对DLBCL具有潜在的诊断价值;在DLBCL中miR-125a-5p上调作用可能影响NF-κB/p65的活化,尤其在Hans分型non-GCB亚型作用明显;在DLBCL中miR-125a-5p的上调可能通过凋亡途径而影响肿瘤的发生发展;miR-125a-5p的高表达可能与DLBCL患者不良预后有关,可作为DLBCL患者预后的独立危险因素。展开更多
目的探讨miR-125a-5p对胰腺癌细胞增殖、凋亡和细胞周期的影响。方法荧光定量PCR检测胰腺癌组织中miR-125a-5p的表达水平,细胞计数试剂盒-8检测下调miR-125a-5p水平对胰腺癌细胞生长的影响,流式细胞术检测下调miR-125a-5p表达水平对胰...目的探讨miR-125a-5p对胰腺癌细胞增殖、凋亡和细胞周期的影响。方法荧光定量PCR检测胰腺癌组织中miR-125a-5p的表达水平,细胞计数试剂盒-8检测下调miR-125a-5p水平对胰腺癌细胞生长的影响,流式细胞术检测下调miR-125a-5p表达水平对胰腺癌细胞周期和凋亡的影响,软琼脂集落形成实验评价miR-125a-5p在胰腺癌细胞恶性转化过程中的作用。结果 miR-125a-5p在胰腺癌组织的表达高于癌旁正常组织(P<0.05)。下调miR-125a-5p表达水平后,胰腺癌细胞系Panc-1和MIA Pa Ca-2的生长受到抑制(P<0.05),早期凋亡率分别增加13.6%和11.0%(P<0.05),细胞集落数目分别下降27.3%和27.8%(P<0.05),Panc-1细胞S期细胞百分比降低11.8%(P<0.05)。结论 miR-125a-5p在胰腺癌组织中高表达,下调miR-125a-5p表达水平使胰腺癌细胞生长受到抑制,集落形成能力下降,细胞周期受到阻滞,凋亡比例增加,提示miR-125a-5p在胰腺癌中发挥癌基因的作用。展开更多
Multiple sclerosis(MS)is a chronic and incurable autoimmune neurodegenerative disease of the central nervous system.Although the symptoms of MS can be managed by vitamin D3 treatment alone,this condition cannot be com...Multiple sclerosis(MS)is a chronic and incurable autoimmune neurodegenerative disease of the central nervous system.Although the symptoms of MS can be managed by vitamin D3 treatment alone,this condition cannot be completely eradicated.Thus,there might be unknown factors capable of regulating the vitamin D receptor(VDR).Genome-wide analysis showed that miRNAs were associated with VDRs.We sought to determine the role and mechanism of action of miRNA-125a-5p and VDRs in a model of MS,mice with experimental autoimmune encephalomyelitis(EAE),which was induced by myelin oligodendrocyte glycoprotein 35–55 peptides.EAE mice showed decreased mean body weight but increased mean clinical scores compared with vehicle or control mice.And inflammatory infiltration was found in the lumbosacral spinal cord of EAE mice.In addition,VDR expression was significantly lower while the expression of miR-125a-5p was markedly higher in the spinal ventral horn of EAE mice than in vehicle or control mice.Importantly,activation of VDRs by paricalcitol or inhibition of miR-125a-5p by its antagomir markedly decreased the mean clinical scores in EAE mice.Interestingly,VDR and miR-125a-5p were co-localized in the same neurons of the ventral horn.More importantly,inhibition of miR-125a-5p remarkably blocked the decrease of VDRs in EAE mice.These results support a critical role for miR-125a-5p in modulating VDR activity in EAE and suggest potential novel therapeutic interventions.展开更多
文摘目的探讨弥漫大B细胞淋巴瘤(DLBCL)中miR-125a-5p的表达水平及与临床病理特征、预后和NF-κB/p65、Bcl2、Caspase3、Ki-67蛋白表达的关系。方法收集84例DLBCL病例,以同期10例淋巴结反应性增生组织作为对照,采用SYBR Green real-time逆转录聚合酶链反应(real-time RT-PCR)检测其miR-125a-5p的表达水平,免疫组化检测NF-κB/p65、Bcl2、Caspase3、Ki-67蛋白表达,收集临床病理资料并随访,结合患者临床资料及预后进行统计学分析。结果在DLBCL样本中miR-125a-5p表达量上调,其表达量是淋巴结反应性增生的(4.99±8.22)倍(P=0.002);miR-125a-5p在DLBCL中的上调与Hans分型non-GCB亚型存在相关性(P=0.027);miR-125a-5p在DLBCL中的上调表达与NF-κB/p65、Bcl2、Caspase3蛋白表达存在显著相关性(P值分别为0.031、0.030、0.022);在DLBCL中Hans分型non-GCB亚型与NF-κB/p65蛋白具有显著相关性(P=0.002);Kaplan-Meier生存分析显示,miR-125a-5p的高表达与DLBCL患者预后有关(P=0.038);多因素Cox分析显示,miR-125a-5p的高表达可能是DLBCL患者预后的独立危险因素(P=0.013)。结论 miR-125a-5p可能对DLBCL具有潜在的诊断价值;在DLBCL中miR-125a-5p上调作用可能影响NF-κB/p65的活化,尤其在Hans分型non-GCB亚型作用明显;在DLBCL中miR-125a-5p的上调可能通过凋亡途径而影响肿瘤的发生发展;miR-125a-5p的高表达可能与DLBCL患者不良预后有关,可作为DLBCL患者预后的独立危险因素。
文摘目的探讨miR-125a-5p对胰腺癌细胞增殖、凋亡和细胞周期的影响。方法荧光定量PCR检测胰腺癌组织中miR-125a-5p的表达水平,细胞计数试剂盒-8检测下调miR-125a-5p水平对胰腺癌细胞生长的影响,流式细胞术检测下调miR-125a-5p表达水平对胰腺癌细胞周期和凋亡的影响,软琼脂集落形成实验评价miR-125a-5p在胰腺癌细胞恶性转化过程中的作用。结果 miR-125a-5p在胰腺癌组织的表达高于癌旁正常组织(P<0.05)。下调miR-125a-5p表达水平后,胰腺癌细胞系Panc-1和MIA Pa Ca-2的生长受到抑制(P<0.05),早期凋亡率分别增加13.6%和11.0%(P<0.05),细胞集落数目分别下降27.3%和27.8%(P<0.05),Panc-1细胞S期细胞百分比降低11.8%(P<0.05)。结论 miR-125a-5p在胰腺癌组织中高表达,下调miR-125a-5p表达水平使胰腺癌细胞生长受到抑制,集落形成能力下降,细胞周期受到阻滞,凋亡比例增加,提示miR-125a-5p在胰腺癌中发挥癌基因的作用。
基金supported by the International Science and Technology Cooperation Plan of Guizhou Province,China[(2013)7027]the National Natural Science Foundation of China(81471137 and 31730040).
文摘Multiple sclerosis(MS)is a chronic and incurable autoimmune neurodegenerative disease of the central nervous system.Although the symptoms of MS can be managed by vitamin D3 treatment alone,this condition cannot be completely eradicated.Thus,there might be unknown factors capable of regulating the vitamin D receptor(VDR).Genome-wide analysis showed that miRNAs were associated with VDRs.We sought to determine the role and mechanism of action of miRNA-125a-5p and VDRs in a model of MS,mice with experimental autoimmune encephalomyelitis(EAE),which was induced by myelin oligodendrocyte glycoprotein 35–55 peptides.EAE mice showed decreased mean body weight but increased mean clinical scores compared with vehicle or control mice.And inflammatory infiltration was found in the lumbosacral spinal cord of EAE mice.In addition,VDR expression was significantly lower while the expression of miR-125a-5p was markedly higher in the spinal ventral horn of EAE mice than in vehicle or control mice.Importantly,activation of VDRs by paricalcitol or inhibition of miR-125a-5p by its antagomir markedly decreased the mean clinical scores in EAE mice.Interestingly,VDR and miR-125a-5p were co-localized in the same neurons of the ventral horn.More importantly,inhibition of miR-125a-5p remarkably blocked the decrease of VDRs in EAE mice.These results support a critical role for miR-125a-5p in modulating VDR activity in EAE and suggest potential novel therapeutic interventions.
