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A Novel Prognostic Biomarker LPAR6 in Hepatocellular Carcinoma via Associating with Immune Infiltrates
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作者 Jian He Mei Meng Hui Wang 《Journal of Clinical and Translational Hepatology》 SCIE 2022年第1期90-103,共14页
Background and Aims:LPAR6 is the most recently deter-mined G protein-coupled receptor of lysophosphatidic acid,and hardly any study has demonstrated the performance of LPAR6 in cancers.We sought to clarify the relatio... Background and Aims:LPAR6 is the most recently deter-mined G protein-coupled receptor of lysophosphatidic acid,and hardly any study has demonstrated the performance of LPAR6 in cancers.We sought to clarify the relationship of LPAR6 to prognosis potential and tumor infiltration im-mune cells in different cancers.Methods:The expression of LPAR6 and its clinical characteristics were evaluated on various databases.The association between LPAR6 and im-mune infiltrates of various types of cancer were investigated via TIMER.Results:We determined that higher LPAR6 ex-pression level was associated with a better overall survival.Additionally,high LPAR6 expression level was significantly associated with better disease-specific survival(DSS)in bladder cancer,and better overall survival(OS)/progres-sion-free survival(PFS)/distant metastasis-free survival(DMFS)/relapse-free survival(RFS)in breast cancer and some other types of cancers.Moreover,LPAR6 significant-ly affects the prognosis of various cancers via The Cancer Genome Atlas(TCGA).Further research exposed that the mRNA level of LPAR6 was positively coordinated with in-filtrating levels of devious immune cells in hepatocellular carcinoma.Conclusions:Our results imply that LPAR6 is associated with prognosis potential and immune infiltration levels in liver cancer.Moreover,LPAR6 expression possibly contributes to the activation of CD8+T,naive T,effector T cells and natural killer cells and inactivates T regulatory cells,decreases T cell exhaustion and regulate T helper cells in liver cancer.These discoveries imply that LPAR6 could be a novel biomarker of prognosis for indicating progno-sis potential and immune-infiltrating level in hepatocellular carcinoma. 展开更多
关键词 lpar6 TILs PROGNOSIS Hepatocellular carcinoma BIOMARKER
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基于网络药理学和实验验证探究丙戊酸致癫痫患儿肥胖的潜在作用机制
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作者 周荣 王俊 +4 位作者 梅艳 李思婵 吴奔红 汪会玲 聂刚 《中国医院药学杂志》 北大核心 2025年第6期644-649,共6页
目的:基于网络药理学、细胞实验及临床样本检测探究丙戊酸(valproic acid,VPA)诱发癫痫患儿肥胖的潜在作用机制。方法:采用网络药理学分析VPA导致肥胖的关键靶点和通路;选取核心靶点与VPA进行分子对接。采用不同浓度的VPA刺激HepG2细胞,... 目的:基于网络药理学、细胞实验及临床样本检测探究丙戊酸(valproic acid,VPA)诱发癫痫患儿肥胖的潜在作用机制。方法:采用网络药理学分析VPA导致肥胖的关键靶点和通路;选取核心靶点与VPA进行分子对接。采用不同浓度的VPA刺激HepG2细胞,CCK-8检测细胞活力,荧光探针检测脂滴含量,油红O染色观察脂肪沉积。收集VPA低、中、高浓度的患者血样,用溶血磷脂酸(lysophosphatidic acid,LPA)酶联免疫吸附试剂盒检测样本中LPA的浓度。结果:网络药理学结果提示VPA导致患儿肥胖的核心靶点是LPAR6,主要作用通路是PI3K-Akt、cAMP信号通路;分子对接结果表明LPAR6与VPA能较好结合。荧光探针检测结果显示,随着VPA的浓度增加,细胞中脂滴增加。油红O染色结果显示VPA可促进细胞内的脂肪沉积,且随着浓度增加,促进作用逐渐增强。临床样本检测结果表明,随着VPA的血药浓度增加,患儿血清中LPA的浓度显著增加。结论:LPA及其受体LPAR6在VPA导致癫痫患儿肥胖中起着关键作用,其机制可能与PI3K-Akt和cAMP信号通路相关。 展开更多
关键词 丙戊酸 癫痫 肥胖 网络药理学 LPA/lpar6
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