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1.
Journal of Clinical Hepatology ; (12): 364-369, 2021.
Article in Chinese | WPRIM | ID: wpr-873407

ABSTRACT

ObjectiveTo investigate the difference in protein expression between hepatocellular carcinoma (HCC) patients with recurrence and those with good prognosis, the differential expression and regulatory mechanism of miR-152-3p target proteins, and the role of miR-152-3p in the recurrence of HCC. MethodsTMT-labeled proteomic sequencing and RT-PCR were used to measure the expression of proteins and the expression of miR-152-3p in the HCC tissue of six patients with recurrence at 2 years after HCC resection and six patients with good prognosis at 5 years. Six databases were used to analyze the target genes of miR-152-3p, and Gene Ontology, DAVID, and REACTOME databases were used to perform target gene screening, enrichment annotation, and signal transduction pathway enrichment analysis. Gene mutation frequency and survival curve analysis were performed for the target genes of miR-152-3p to verify the role of miR-152-3p target genes in patients with HCC recurrence. The independent samples t-test was used for comparison of continuous data between two groups, and a Kaplan-Meier analysis was performed to investigate the survival rates of liver-related genes. ResultsCompared with the patients with HCC recurrence, the patients with good prognosis after HCC resection had a significantly higher transcriptional expression level of miR-152-3p in HCC tissue (P<0.05). The results of protein sequencing showed that there were 365 differentially expressed proteins in HCC tissue between the patients with good prognosis and the patients with recurrence, and the analysis of HCC recurrence databases showed that 17 proteins were regulated by miR-152-3p. Further analysis of the signaling pathways showed that the function of the 17 target genes regulated by miR-152-3p was enriched in the translation and regulation of mitochondria and ribosome, and multiple enrichment revealed that six target genes were closely associated with mitochondrial respiratory chain complex, i.e., AKAP1, FOXRED1, MRPL28, MRPL50, SHC1, and STAU1. Gene mutation frequency and survival curve analysis showed that the loss or weakening of the function of mitochondrial respiratory chain-related target proteins seriously affected the prognosis and survival rate of patients. ConclusionThere is a significant difference in the expression of miR-152-3p in HCC tissue between patients with good prognosis and those with recurrence after HCC resection, and miR-152-3p may lead to the recurrence of HCC by regulating the target genes AKAP1, FOXRED1, MRPL28, MRPL50, SHC1, and STAU1, acting on the mitochondrial respiratory chain, and affecting the oxidative respiratory function of cells.

2.
Journal of Central South University(Medical Sciences) ; (12): 316-320, 2008.
Article in Chinese | WPRIM | ID: wpr-814077

ABSTRACT

OBJECTIVE@#To investigate whether there is association between the-2548G/A functional polymorphism in the promoter region of leptin gene and weight gain following antipsychotic agents (APS) acute treatment in schizophrenic patients.@*METHODS@#Eight-four Chinese Han untreated schizophrenia patients in 70 nuclear families were recruited. The polymorphism of leptin gene was determined with PCR-RFLP technique. Body weight was measured in the patients on admission the and after 10 weeks treatment with risperidone or chlorpromazine.@*RESULTS@#There was an average (8.00+/-6.13)% increases in baseline weight after the 10 week treatment. There were significant differences in the distribution of allele frequencies (chi2=4.031, P=0.045) between the patients with weight changed >or=7% and <7% subgroups. Family-based association analysis further confirmed the above significant finding by transmission disequilibrium test but not by quantitative trait transmission disequilibrium test.@*CONCLUSION@#The finding confirms that the-2548G/A polymorphism in promoter region of leptin gene is associated with APS-induced weight gain.


Subject(s)
Adolescent , Adult , Female , Humans , Male , Antipsychotic Agents , Therapeutic Uses , Family Health , Genotype , Leptin , Genetics , Polymerase Chain Reaction , Polymorphism, Restriction Fragment Length , Promoter Regions, Genetic , Genetics , Schizophrenia , Drug Therapy , Genetics , Weight Gain , Genetics
3.
Chinese Journal of Medical Genetics ; (6): 575-576, 2005.
Article in Chinese | WPRIM | ID: wpr-279996

ABSTRACT

<p><b>OBJECTIVE</b>To investigate whether the -1438G/A polymorphism in the promoter region of 5-HTR2A gene associates with the weight gain following antipsychotic agents (APS) acute treatment in schizophrenic patients.</p><p><b>METHODS</b>Eighty-four Chinese Han patients with schizophrenia at the first onset were recruited from among 70 nuclear families. The polymorphism of 5-HTR2A gene was determined with PCR-RFLP technique. Body weight was measured in the patients on admission after 10 weeks of treatment with risperidone or chlorpromazine.</p><p><b>RESULTS</b>There were no statistically significant differences in the distribution frequencies of genotype (chi2: 0.172, v1, P > 0.05) and allele (chi2: 0.121, v1, P > 0.05) of -1438G/A polymorphism of 5-HTR2A gene between subgroups (weight gain >or= 7% or < 7%). Likewise, there was no significant difference in weight gain between genotype groups. By means of transmission disequilibrium test and quantitative transmission disequilibrium test, no significant association between the -1438G/A polymorphism of 5-HTR2A gene and weight gain was observed.</p><p><b>CONCLUSION</b>5-HTR2A gene -1438G/A polymorphism was probably not associated with APS-induced weight gain in Chinese Han patients with schizophrenia in this study.</p>


Subject(s)
Adult , Female , Humans , Male , Antipsychotic Agents , Therapeutic Uses , Chlorpromazine , Therapeutic Uses , Gene Frequency , Genotype , Polymerase Chain Reaction , Polymorphism, Genetic , Polymorphism, Restriction Fragment Length , Promoter Regions, Genetic , Genetics , Receptor, Serotonin, 5-HT2A , Genetics , Risperidone , Therapeutic Uses , Schizophrenia , Drug Therapy , Genetics , Weight Gain , Genetics
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