目的探讨染色体区域稳定蛋白1(chromosomal region maintenance 1,CRM1)与细胞因子信号传导抑制因子1(suppressor of cytokine signaling 1,SOCS1)表达与胃癌演进、临床病理特征及预后的关系。方法采用免疫组化检测低级别上皮内瘤变胃组...目的探讨染色体区域稳定蛋白1(chromosomal region maintenance 1,CRM1)与细胞因子信号传导抑制因子1(suppressor of cytokine signaling 1,SOCS1)表达与胃癌演进、临床病理特征及预后的关系。方法采用免疫组化检测低级别上皮内瘤变胃组织27例、高级别上皮内瘤变胃组织26例,以及进展期胃癌组织67例及对应癌旁组织67例中CRM1及SOCS1蛋白表达水平,分析两者在不同病变胃黏膜中的变化以及与胃癌临床病理特征的关系,通过在线分析工具Kaplan-Meier Plotter、单因素及多因素Cox分析影响胃癌患者预后的相关因素。结果胃癌组织中CRM1表达高于癌旁组织,SOCS1表达低于癌旁组织及瘤变组织(P<0.05);CRM1在胃癌组织高表达与浸润深度及淋巴结转移有关(P<0.05);生存分析显示高表达CRM1提示预后不良(P<0.05),SOCS1表达水平与预后无关(P>0.05);在胃癌组织中,CRM1与SOCS1表达无显著相关性(R=-0.025,P=0.842)。结论CRM1和SOCS1参与胃癌发生,CRM1高表达可能参与胃癌侵袭及转移等恶性进展。展开更多
The low intrinsic growth capacity of neurons and an injury-induced inhibitory milieu are major contributo rs to the failure of sensory and motor functional recovery following spinal cord injury.Heat shock transcriptio...The low intrinsic growth capacity of neurons and an injury-induced inhibitory milieu are major contributo rs to the failure of sensory and motor functional recovery following spinal cord injury.Heat shock transcription factor 1(HSF1),a master regulator of the heat shock response,plays neurogenetic and neuroprotective roles in the damaged or diseased central nervous system.However,the underlying mechanism has not been fully elucidated.In the present study,we used a gecko model of spontaneous nerve regeneration to investigate the potential roles of gecko HSF1(gHSF1) in the regulation of neurite outgrowth and inflammatory inhibition of macrophages following spinal cord injury.gHSF1 expression in neurons and microglia at the lesion site increased dramatically immediately after tail amputation.gHSF1 ove rexpression in gecko primary neuro ns significantly promoted axonal growth by suppressing the expression of suppressor of cytokine signaling-3,and fa cilitated neuro nal survival via activation of the mitogen-activated extracellular signal-regulated kinase/extracellular regulated protein kinases and phosphatidylinositol 3-kinase/protein kinase B pathways.Furthermore,gHSF1 efficiently inhibited the macrophagemediated inflammatory response by inactivating 1kappa B-alpha/NF-kappaB signaling.Our findings show that HSF1 plays dual roles in promoting axonal regrowth and inhibiting leukocyte inflammation,and provide new avenues of investigation for promoting spinal co rd injury repair in mammals.展开更多
文摘目的探讨染色体区域稳定蛋白1(chromosomal region maintenance 1,CRM1)与细胞因子信号传导抑制因子1(suppressor of cytokine signaling 1,SOCS1)表达与胃癌演进、临床病理特征及预后的关系。方法采用免疫组化检测低级别上皮内瘤变胃组织27例、高级别上皮内瘤变胃组织26例,以及进展期胃癌组织67例及对应癌旁组织67例中CRM1及SOCS1蛋白表达水平,分析两者在不同病变胃黏膜中的变化以及与胃癌临床病理特征的关系,通过在线分析工具Kaplan-Meier Plotter、单因素及多因素Cox分析影响胃癌患者预后的相关因素。结果胃癌组织中CRM1表达高于癌旁组织,SOCS1表达低于癌旁组织及瘤变组织(P<0.05);CRM1在胃癌组织高表达与浸润深度及淋巴结转移有关(P<0.05);生存分析显示高表达CRM1提示预后不良(P<0.05),SOCS1表达水平与预后无关(P>0.05);在胃癌组织中,CRM1与SOCS1表达无显著相关性(R=-0.025,P=0.842)。结论CRM1和SOCS1参与胃癌发生,CRM1高表达可能参与胃癌侵袭及转移等恶性进展。
基金supported by the National Natural Science Foundation of China,No.31871211 (to YJunW)the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)。
文摘The low intrinsic growth capacity of neurons and an injury-induced inhibitory milieu are major contributo rs to the failure of sensory and motor functional recovery following spinal cord injury.Heat shock transcription factor 1(HSF1),a master regulator of the heat shock response,plays neurogenetic and neuroprotective roles in the damaged or diseased central nervous system.However,the underlying mechanism has not been fully elucidated.In the present study,we used a gecko model of spontaneous nerve regeneration to investigate the potential roles of gecko HSF1(gHSF1) in the regulation of neurite outgrowth and inflammatory inhibition of macrophages following spinal cord injury.gHSF1 expression in neurons and microglia at the lesion site increased dramatically immediately after tail amputation.gHSF1 ove rexpression in gecko primary neuro ns significantly promoted axonal growth by suppressing the expression of suppressor of cytokine signaling-3,and fa cilitated neuro nal survival via activation of the mitogen-activated extracellular signal-regulated kinase/extracellular regulated protein kinases and phosphatidylinositol 3-kinase/protein kinase B pathways.Furthermore,gHSF1 efficiently inhibited the macrophagemediated inflammatory response by inactivating 1kappa B-alpha/NF-kappaB signaling.Our findings show that HSF1 plays dual roles in promoting axonal regrowth and inhibiting leukocyte inflammation,and provide new avenues of investigation for promoting spinal co rd injury repair in mammals.
