| 3 | Genetic variants in promoter region of TFR2 is associated with the risk of non-alcoholic fatty liver disease in a Chinese Han population:a case–control study显示文摘Background Iron overload is frequently observed in non-alcoholic fatty liver disease(NAFLD).Transferrin receptor 2(TFR2)is an important key factor in iron regulation.We aimed to investigate whether TFR2 single nucleotide polymorphisms(SNPs)contribute to susceptibility to NAFLD in a Chinese Han population.Methods Five tag SNPs(rs10247962,rs4434553,rs2075672,rs1052897,and rs3757859)in the TFR2 gene were selected and genotyped in a case–control study on participants who visited two affiliated hospitals of Fujian Medical University between June 2011 and August 2017.Propensity score matching and inverse probability of treatment weighting analyses were used to verify the risk associated with TFR2 SNPs.Results Logistic regression analyses suggested that subjects with the rs4434553 GA or GG genotype had a lower risk of NAFLD than those carrying the AA genotype(odds ratio=0.630,95%confidence interval=0.504–0.788).Moreover,the rs4434553 GA or GG genotype was negatively correlated with body mass index,hepatic steatosis index,and serum ferritin(b=-0.363,P=0.008;b=-1.040,P=0.009;b=-35.258,P=0.015,respectively),and positively associated with serum hepcidin level(b=35.308,P<0.001).Moreover,rs10247962 and rs1052897 had multiplicative interactions with age in relation to the risk of NAFLD(P for interactions,0.041 and 0.034,respectively).The cumulative effects of the rs10247962,rs1052897,and rs4434553 SNPs were positively associated with the risk of NAFLD(adjusted P_(trend)=0.012).Conclusions In this Chinese Han population,the rs4434553 polymorphism in TFR2 may be an independent influencing factor associated with the susceptibility to NAFLD.The ageing effect on the development of NAFLD may be inhibited by SNPs rs10247962 and rs1052897. | Xinting Pan Hewei Peng Junchao Zhang Yunli Wu Zhijian Hu Xian-E.Peng | 2022 | Gastroenterology Report2022，10，1： | 0 |
| 4 | Recombinant adenovirus vector-mediated human MDA-7 gene transfection suppresses hepatocellular carcinoma growth in a mouse xenograft model显示文摘Hepatocellular carcinoma is one of the most common tumors in the world.The purpose of the present study was to investigate the inhibitory effects of adenoviral transduction of human melanoma differentiation-associated gene-7(MDA-7)gene on hepatocellular carcinoma,so as to provide a theoretical basis for gene therapy of the disease.The human MDA-7 gene was cloned into replication-defective adenovirus specific to HepG2 cells using recombinant virus technology.RT-PCR and Western blotting assays were used to determine the expression of human MDA-7 mRNA and MDA-7 protein in HepG2 cells in vitro.Induction of apoptosis by overexpression of the human MDA-7 gene was determined by flow cytometry.In-vivo efficacy of adenoviral delivery of the human MDA-7 gene was assessed in nude mice bearing HepG2 cell lines in vivo by determining inhibition of tumor growth,VEGF and CD34 expression,and microvascular density(MVD).The results showed that AdGFP/MDA-7 induced apoptosis of HepG2 cells in vitro and significantly inhibited tumor growth in vivo(P < 0.05).The intra-tumoral MVD decreased significantly in the treated tumors(P < 0.05).We conclude the recombination adenovirus AdGFP/MDA-7 can effectively express biologically active human MDA-7,which leads to inhibition of hepatocellular carcinoma growth. | Xinting Pan Liqun Wu Jingyu Cao Weidong Guo Zusen Wang Bing Han Weiyu Hu | 2012 | The Journal of Biomedical Research2012，26，1： | 0 |
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