GPSM2 Signal Transduction Computational Network Analysis in Human No-Tumor Hepatitis/Cirrhosis and Hepatocellular Carcinoma Transformation
首发时间:2018-08-28
Abstract:LGN protein (GPSM2) is involved in transcription or cell division presented in several papers. However, how the molecular network and interpretation concerning GPSM2 signal transduction between no-tumor hepatitis/cirrhosis and hepatocellular carcinoma (HCC) transformation remains to be elucidated. Here we constructed and analyzed significant higher expression gene GPSM2 activated & inhibited upstream and downstream signal transduction network from HCC vs no-tumor hepatitis/cirrhosis pateints (viral infection HCV or HBV) in GEO Dataset by using gene regulatory network inference method based on linear programming and decomposition procedure, under covering GPSM2 pathway and matching signal transduction enrichment analysis by the CapitalBio MAS 3.0 integrated of public databases including Gene Ontology, KEGG, BioCarta, GenMapp, Intact, UniGene, OMIM, etc. By compared the different activated & inhibited GPSM2 network with GO analysis between no-tumor hepatitis/cirrhosis and HCC transformation, our result showed GPSM2 signal transduction network: (1) more nucleus and cytoplasm but less extracellular space protein binding in no-tumor hepatitis/cirrhosis; (2) more growth factor activity but less cytoplasm enzyme activator activity in HCC; (3) less activation & more inhibition molecular numbers in no-tumor hepatitis/cirrhosis but more activation & less inhibition in HCC. Therefore, we inferred (4) GPSM2 signal transduction network stronger transcription but weaker cell differentiation as a result increasing cytoplasm protein translation in no-tumor hepatitis/cirrhosis; (5) stronger cell proliferation but weaker regulation of muscle contraction as a result inceasing nuclear cell division in HCC.
keywords: LGN protein (GPSM2) computational network signal transduction human hepatocellular carcinoma transformation no-tumor hepatitis/cirrhosis
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GPSM2在非肿瘤肝炎肝硬化组织和肝癌之间的信号转导计算网络分析
摘要:许多论文中提到LGN蛋白(GPSM2)参与转录或细胞分裂。然而,非肿瘤肝炎/肝硬化和肝癌(HCC)转化之间的GPSM2信号转导的分子网络和解释仍有待阐明。本文采用GEO数据集通过基于GO,KEGG,GenMAPP,BioCarta,Intact,UniGene,OMIM和Disease等的整合分析的分子注释系统MAS使GPSM2的网络覆盖并匹配其通路进行信号转导的富集度分析,然后通过GRNInfer算法对比分析了肝癌样本与非肿瘤肝炎及肝硬化样本,构建了GPSM2的激活和抑制的上下游信号转导网络,最后通过GO分析比较了非肿瘤肝炎/肝硬化和肝癌之间转化的GPSM2激活与抑制网络的不同。根据实验结果,得出GPSM2信号转导网络的五点结论:(1)在非肿瘤肝炎/肝硬化中,显示更多的细胞核和细胞质以及较少的细胞外空隙蛋白质结合;(2)在肝癌中表现出较强的生长因子活性和较弱的胞浆酶活化剂活性;(3)在非肿瘤肝炎/肝硬化中体现较少的激活分子数量和较多抑制分子数量,然而在肝癌中显示较多的激活分子和较少的抑制分子数量。(4)因此,我们推断在非肿瘤肝炎/肝硬化中,GPSM2信号转导网络具备更强大的转录功能但较弱的细胞分化特性,从而能增加细胞质蛋白质的转化;(5)在肝癌中体现更强的细胞增殖同时较弱的肌肉收缩的规律,从而提高核细胞分裂。
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GPSM2在非肿瘤肝炎肝硬化组织和肝癌之间的信号转导计算网络分析
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