Why MUC16 mutations lead to a better prognosis: A study based on The Cancer Genome Atlas gastric cancer cohort

BACKGROUND MUC16, encoding cancer antigen 125, is a frequently mutated gene in gastric cancer. In addition, MUC16 mutations seem to result in a better prognosis in gastric cancer. However, the mechanisms that lead to a better prognosis by MUC16 mutations have not yet been clarified.AIMTo delve deeper into the underlying mechanisms that explain why MUC16 mutations signal a better prognosis in gastric cancer.METHODSWe used multi-omics data, including mRNA, simple nucleotide variation, copy number variation and methylation data from The Cancer Genome Atlas, to explore the relationship between MUC16 mutations and prognosis. Cox regression and random survival forest algorithms were applied to search for hub genes. Gene set enrichment analysis was used to elucidate the molecular mechanisms. Single-sample gene set enrichment analysis and “EpiDISH” were used to assess immune cells infiltration, and “ESTIMATE” for analysis of the tumor microenvironment.RESULTSOur study found that compared to the wild-type group, the mutation group had a better prognosis. Additional analysis indicated that the MUC16 mutations appear to activate the DNA repair and p53 pathways to act as an anti-tumor agent. We also identified a key gene, NPY1R (neuropeptide Y receptor Y1), which was significantly more highly expressed in the MUC16 mutations group than in the MUC16 wild-type group. The high expression of NPY1R predicted a poorer prognosis, which was also confirmed in a separate Gene Expression Omnibus cohort. Further susceptibility analysis revealed that NPY1R might be a potential drug target for gastric cancer. Furthermore, in the analysis of the tumor microenvironment, we found that immune cells in the mutation group exhibited higher anti-tumor effects. In addition, the tumor mutation burden and cancer stem cells index were also higher in the mutation group than in the wild-type group.CONCLUSIONWe speculated that the MUC16 mutations might activate the p53 pathway and DNA repair pathway: alternatively, the tumor microenvironment may be involved.     

Role of cytochrome epoxygenase (CYP2J2) in the pathophysiology of coronary artery disease in South Indian population

Background

The cytochrome P-450 2J2 (CYP2J2) is known to be one of the major enzymes of epoxygenase pathway of arachidonic acid in extrahepatic tissues, which produces series of regioisomeric cis-epoxyeicosatrienoic acids (EETs) such as 5,6-, 8,9-, 11,12-, and 14,15-EETs. In the present study, we analyzed the impact of a genetic variant in CYP2J2 on coronary artery disease (CAD) in the Telangana region of Indian population.

构建不同筛选特性的HBV X基因真核表达载体

目的:构建不同筛选特性的两个HBV X基因真核表达载体.方法:从质粒pEcob6中PCR扩增HBV X全基因,利用pCEP4和pcDNA3.1( )两者多克隆位点的特点,选用pGEM(R)-T Easy Vector构建中间载体pEasy-X,分别酶切后连接特异性片段构建载体pCEP4-X和pcDNA3.1( )-X.结果:从质粒pEcob6成功PCR扩增出HBV X全基因并克隆至质粒pEasy-X,酶切、PCR及测序均证实真核表达载体质粒pCEP4-X和pcDNA3.1( )-X构建成功.结论:具有不同筛选特性的两个HBVX基因真核表达载体业已成功构建.     

长链非编码RNA LOXL1-AS1在胃癌中的表达及其临床意义

目的探讨lncRNA LOXL1-AS1在胃癌中的表达及其临床意义。方法实时荧光PCR(qRT-PCR)检测89对胃癌组织及癌旁组织标本中lncRNA LOXL1-AS1的表达情况,并分析其与各临床病理因素的相关性;利用Kaplan Meier plotter数据库分析不同LOXL1-AS1表达状态下胃癌患者的总生存率差异,探讨LOXL1-AS1表达评估胃癌患者预后的价值。结果胃癌组织LOXL1-AS1表达量显著高于癌旁组织(P<0.05);胃癌组织中LOXL1-AS1表达量与患者肿瘤直径、局部淋巴结转移、远处转移和TNM分期密切相关(P<0.05),但与患者年龄、性别、腹膜转移、肿瘤分化程度等无相关性(P>0.05);Kaplan Meier plotter数据库纳入分析了631例病例样本,其中455例为高表达,176例为低表达。LOXL1-AS1高表达组胃癌患者生存率显著低于LOXL1-AS1低表达组患者,差异有统计学意义(HR=1.52,95%CI:1.17~1.97,P=0.0014)。结论LOXL1-AS1在胃癌中高表达,可能参与了胃癌发生、发展过程;LOXL1-AS1可能作为预测胃癌患者预后评估的指标。     

流感病毒血凝素在多种系统中表达的研究进展

流感疫苗是预防流感病毒感染最有效的方法。传统灭活流感疫苗通过在鸡胚中培养病毒后经纯化获得。流感每年都会发生季节性流行,流感病毒高度多变的特性使生产有效疫苗成为一项挑战。为了克服流感疫苗生产对鸡胚的依赖,需要开发新的流感疫苗生产策略。由于血凝素是流感病毒主要表面抗原之一,重组血凝素亚单位疫苗为流感疫苗的生产提供了一个方案。本文将对流感病毒血凝素在大肠埃希菌、毕赤酵母、昆虫细胞、哺乳动物细胞多种系统中表达的研究进行综述。