目的:探讨三结构域蛋白家族24(tripartite motif-containing protein 24,TRIM24)、c-myc及ARF蛋白在食管鳞状细胞癌组织中的表达及其意义。方法:选取2018年01月至2022年12月期间承德市中心医院接受手术治疗的102例食管鳞癌患者临床病理...目的:探讨三结构域蛋白家族24(tripartite motif-containing protein 24,TRIM24)、c-myc及ARF蛋白在食管鳞状细胞癌组织中的表达及其意义。方法:选取2018年01月至2022年12月期间承德市中心医院接受手术治疗的102例食管鳞癌患者临床病理资料作为研究对象(实验组),同时选取癌旁正常食管黏膜组织54例(对照组),采用免疫组化(Envision法)对TRIM24、c-myc及ARF蛋白进行检测,观察三者在鳞癌组织及癌旁正常食管黏膜组织中的表达情况,并分析三者的表达与临床病理特征的关系,同时研究三者于食管鳞癌组织内表达的相关性。结果:TRIM24、c-myc及ARF在鳞癌组织及癌旁正常食管黏膜组织中阳性表达率分别为72.62%vs 7.45%、74.36%vs 13.85%、26.56%vs 83.18%,三种蛋白在鳞癌组织及正常食管黏膜组织中的表达差异具有统计学意义(P均<0.05);经分析,食管鳞癌组织中的TRIM24、c-myc及ARF蛋白表达与癌的分化程度、淋巴结转移、临床分期具有显著相关性(P均<0.05);经Spearman相关性分析,食管鳞癌组织中TRIM24与c-myc蛋白表达呈正相关(r=0.587,P<0.05),TRIM24与ARF蛋白表达呈负相关(r=-0.601,P<0.05),c-myc与ARF蛋白表达呈负相关(r=-0.465,P<0.05)。结论:TRIM24、c-myc、ARF的异常表达可能对食管鳞状细胞癌的发生及发展有一定关系。因此,c-myc、TRIM24和ARF可能作为新的潜在治疗靶点,为食管鳞癌患者的个体化治疗提供新的方向。展开更多
目的本研究旨在探讨姜黄素对结肠癌RKO细胞增殖的抑制作用及其机制,重点关注三结构域蛋白2(tripartite motif-containing protein 2,TRIM2)表达和哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)信号通路的调控。方法通过...目的本研究旨在探讨姜黄素对结肠癌RKO细胞增殖的抑制作用及其机制,重点关注三结构域蛋白2(tripartite motif-containing protein 2,TRIM2)表达和哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)信号通路的调控。方法通过分析计算半数抑制浓度(half maximal inhibitory concentration,IC50)值,确定实验姜黄素给药浓度。采用实时荧光定量聚合酶链式反应(quantitative polymerase chain reaction,qPCR)法检测RKO细胞和人正常肠黏膜细胞(fetal human colon,FHC)中TRIM2表达水平。通过蛋白质免疫印迹实验(Western blotting,WB)检测姜黄素处理后RKO细胞中TRIM2及敲减TRIM2后RKO细胞mTOR通路相关蛋白表达情况。利用细胞计数试剂盒(cell counting kit-8,CCK8)检测姜黄素处理、TRIM2敲减及mTOR信号通路激活剂对RKO细胞增殖的影响。结果TRIM2在RKO细胞中异常高表达。姜黄素可降低RKO细胞TRIM2表达,敲减TRIM2后RKO细胞mTOR信号通路相关蛋白表达下调。姜黄素和TRIM2敲减均显著抑制RKO细胞增殖,而mTOR信号通路激活剂可逆转这种抑制作用。结论姜黄素通过下调TRIM2表达调控mTOR信号通路抑制结肠癌RKO细胞增殖。展开更多
特发性肺纤维化(IPF)是一种进行性且最终致命的纤维化肺病,可以导致进行性的肺功能下降,其发展被认为与遗传、环境、免疫、炎症、自噬、衰老等因素有关。TRIM蛋白是一个高度保守的E3泛素连接酶家族,参与多个过程:包括细胞内信号传导、...特发性肺纤维化(IPF)是一种进行性且最终致命的纤维化肺病,可以导致进行性的肺功能下降,其发展被认为与遗传、环境、免疫、炎症、自噬、衰老等因素有关。TRIM蛋白是一个高度保守的E3泛素连接酶家族,参与多个过程:包括细胞内信号传导、发育、细胞凋亡、蛋白质质量控制、先天免疫、自噬和致癌作用,近年来,有关TRIM蛋白在疾病中的研究越来越多,研究表明它们可以参与细胞内信号传导、发育、细胞凋亡、蛋白质质量控制、先天免疫、自噬和致癌等多个过程,它们的失调会导致癌症、免疫疾病或发育障碍等疾病,参考肺纤维化所涉及的发生发展机制,TRIM蛋白在各器官纤维化中的研究也逐渐展开,本文将主要论述TRIM蛋白在肺纤维化中的研究进展。Idiopathic pulmonary fibrosis (IPF) is a progressive and ultimately fatal fibrotic lung disease that can lead to progressive decline in lung function, and its development is thought to be related to genetic, environmental, immune, inflammatory, autophagy, aging and other factors. TRIM proteins are a highly conserved family of E3 ubiquitin ligases involved in several processes: It includes intracellular signaling, development, apoptosis, protein quality control, innate immunity, autophagy and carcinogenesis. In recent years, more and more studies on TRIM proteins in diseases have shown that they can participate in many processes such as intracellular signaling, development, apoptosis, protein quality control, innate immunity, autophagy and carcinogenesis. Their disorders can lead to cancer, immune diseases or developmental disorders and other diseases, referring to the occurrence and development mechanism involved in pulmonary fibrosis, the study of TRIM protein in various organ fibrosis is also gradually launched, this paper will mainly discuss the research progress of TRIM protein in pulmonary fibrosis.展开更多
文摘MG53(mitsugumin 53)蛋白,是E3泛素连接酶多功能三结构域(tripartite motif,TRIM)蛋白家族成员之一,又被称为TRIM72。MG53是一种细胞膜修复蛋白,广泛表达于心肌和骨骼肌,可在膜损伤部位快速积累,在骨骼肌和心肌细胞膜修复中发挥重要作用。近年来,大量研究发现,MG53可以参与缺血预适应和缺血后适应的心肌保护作用,减轻心肌缺血再灌注损伤;并且在生理或病理状态下,MG53在许多器官中均有表达,促进细胞膜修复。然而MG53过表达则会导致泛素依赖的胰岛素受体表达下降,进而导致代谢综合征和糖尿病性心脏病。本文综述了近年来MG53的生理功能及其相关作用机制研究进展,以期为重组人MG53(recombinant human mitsugumin53,rhMG53)的临床应用提供参考。
文摘特发性肺纤维化(IPF)是一种进行性且最终致命的纤维化肺病,可以导致进行性的肺功能下降,其发展被认为与遗传、环境、免疫、炎症、自噬、衰老等因素有关。TRIM蛋白是一个高度保守的E3泛素连接酶家族,参与多个过程:包括细胞内信号传导、发育、细胞凋亡、蛋白质质量控制、先天免疫、自噬和致癌作用,近年来,有关TRIM蛋白在疾病中的研究越来越多,研究表明它们可以参与细胞内信号传导、发育、细胞凋亡、蛋白质质量控制、先天免疫、自噬和致癌等多个过程,它们的失调会导致癌症、免疫疾病或发育障碍等疾病,参考肺纤维化所涉及的发生发展机制,TRIM蛋白在各器官纤维化中的研究也逐渐展开,本文将主要论述TRIM蛋白在肺纤维化中的研究进展。Idiopathic pulmonary fibrosis (IPF) is a progressive and ultimately fatal fibrotic lung disease that can lead to progressive decline in lung function, and its development is thought to be related to genetic, environmental, immune, inflammatory, autophagy, aging and other factors. TRIM proteins are a highly conserved family of E3 ubiquitin ligases involved in several processes: It includes intracellular signaling, development, apoptosis, protein quality control, innate immunity, autophagy and carcinogenesis. In recent years, more and more studies on TRIM proteins in diseases have shown that they can participate in many processes such as intracellular signaling, development, apoptosis, protein quality control, innate immunity, autophagy and carcinogenesis. Their disorders can lead to cancer, immune diseases or developmental disorders and other diseases, referring to the occurrence and development mechanism involved in pulmonary fibrosis, the study of TRIM protein in various organ fibrosis is also gradually launched, this paper will mainly discuss the research progress of TRIM protein in pulmonary fibrosis.
