Although previous studies showed that the principal oncoprotein encoded by Epstein-Barr virus, latent membrane protein 1 (LMP1), could induce the nasopharyngeal carcinoma cells in G2/M phase increased, littleis known ...Although previous studies showed that the principal oncoprotein encoded by Epstein-Barr virus, latent membrane protein 1 (LMP1), could induce the nasopharyngeal carcinoma cells in G2/M phase increased, littleis known about the target molecules and mechanisms. The present study demonstrated that LMP1 couldinduce the accumulation of p53 protein and upregulate its transactivity in a dose dependent manner, whichresulted in the decrease of the kinase activity of cdc2/cyclin B complex and inducing arrest at G2/M phasethrough the activation of NF-kB and AP-1 signaling pathways, and the effect of NF-kB was more obviousthan that of AP-1. This study provided some significant evidence for further elucidating the molecular mechanisms that LMP1 had effects on the surveillance mechanism of cell cycle and promoting the survivalof transformed cells and tumorigenesis.展开更多
Previous work has demonstrated that the sensitization of spinal neurons and microglia is important in the development of pain behaviors induced by BmK I,a Na^+ channel activator and a major peptide component of the ve...Previous work has demonstrated that the sensitization of spinal neurons and microglia is important in the development of pain behaviors induced by BmK I,a Na^+ channel activator and a major peptide component of the venom of the scorpion Buthus martensi Karsch(BmK).We found that the expression of P2X7 receptors(P2X7Rs)was up-regulated in the ipsilateral spinal dorsal horn after BmK I injection in rats.P2X7R was selectively localized in microglia but not astrocytes or neurons.Similarly,interleukin 1β(IL-1β)was selectively up-regulated in microglia in the spinal dorsal horn after BmK I injection.Intrathecal injection of P2X7R antagonists largely reduced BmK I-induced spontaneous and evoked pain behaviors,and the up-regulation of P2X7R and IL-1β in the spinal cord.These data suggested that the up-regulation of P2X7Rs mediates microglial activation in the spinal dorsal horn,and therefore contributes to the development of BmK I-induced pain.展开更多
文摘目的:探讨CXCR1/CXCR2受体拮抗剂-G31P对人前列腺癌细胞PC-3增殖的体内外抑制作用。方法:采用CCK-8法研究不同浓度G31P对PC-3细胞体外增殖的抑制作用。建立体内绿色荧光蛋白(Green fluorescent protein,GFP)标记人雄激素非依赖性前列腺癌细胞PC-3裸鼠原位移植瘤模型,观察G31P对裸鼠前列腺癌原位移植瘤的体积、重量的影响。结果:CCK-8结果显示100 ng/ml G31P与对照组相比分别作用1、3 d和5 d差异具有统计学意义(1 d P=0.007、3 d P=0.001、5 d P=0.028,均为P<0.05)。前列腺癌PC-3细胞裸鼠模型体内实验显示,与对照组(100μl N.S)相比,G31P处理组(0.5 mg/kg)从给药第18天起能显著抑制前列腺肿瘤的体积(P=0.026,P<0.05);与对照组相比G31P处理组在抑制前列腺肿瘤重量方面有明显作用(P=0.027,P<0.05)。结论:G31P体内外实验均能抑制人雄激素非依赖性前列腺癌细胞系PC-3的增殖。
文摘Although previous studies showed that the principal oncoprotein encoded by Epstein-Barr virus, latent membrane protein 1 (LMP1), could induce the nasopharyngeal carcinoma cells in G2/M phase increased, littleis known about the target molecules and mechanisms. The present study demonstrated that LMP1 couldinduce the accumulation of p53 protein and upregulate its transactivity in a dose dependent manner, whichresulted in the decrease of the kinase activity of cdc2/cyclin B complex and inducing arrest at G2/M phasethrough the activation of NF-kB and AP-1 signaling pathways, and the effect of NF-kB was more obviousthan that of AP-1. This study provided some significant evidence for further elucidating the molecular mechanisms that LMP1 had effects on the surveillance mechanism of cell cycle and promoting the survivalof transformed cells and tumorigenesis.
基金supported by grants from the National Natural Science Foundation of China (31571032 and 31771191)supported by an Indiana Spinal Cord and Brain Injury Research Fund grant from Indiana State Department of Health, USA (2017)
文摘Previous work has demonstrated that the sensitization of spinal neurons and microglia is important in the development of pain behaviors induced by BmK I,a Na^+ channel activator and a major peptide component of the venom of the scorpion Buthus martensi Karsch(BmK).We found that the expression of P2X7 receptors(P2X7Rs)was up-regulated in the ipsilateral spinal dorsal horn after BmK I injection in rats.P2X7R was selectively localized in microglia but not astrocytes or neurons.Similarly,interleukin 1β(IL-1β)was selectively up-regulated in microglia in the spinal dorsal horn after BmK I injection.Intrathecal injection of P2X7R antagonists largely reduced BmK I-induced spontaneous and evoked pain behaviors,and the up-regulation of P2X7R and IL-1β in the spinal cord.These data suggested that the up-regulation of P2X7Rs mediates microglial activation in the spinal dorsal horn,and therefore contributes to the development of BmK I-induced pain.
