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1.
Zhonghua Nan Ke Xue ; 27(8): 675-679, 2021 Aug.
Artigo em Chinês | MEDLINE | ID: mdl-34914237

RESUMO

OBJECTIVE: To analyze the effects of high-fat diet on the biological network regulation of gene expression microarray data and key proteins in mouse prostate tissue, and provide some new theoretical evidence for the mechanism of obesity inducing PCa. METHODS: From the Gene Expression Omnibus (GEO), we obtained RNAs in the prostate tissue from two groups of C57BL / 6J mice, the normal diet group (n = 5) and high-fat diet group (n = 4). Using the Gene Cloud, Gene-Cloud of Biotechnology Informs (GCBI), GenClip2.0, and Sytoscape 3.5.1, we screened differentially expressed genes, investigated protein interaction networks and biological pathways of differential genes and, from the perspective of transcriptome, explored the effects of high-fat diet on the changes of the molecular network of prostate tissue genes and the molecular biological functions possibly involved. RESULTS: A total of 134 differentially expressed genes were identified, 130 up-regulated and 4 down-regulated, mainly involved in biological functions such as chromosome organization, cell-cell signaling, small molecule biosynthesis and leukocyte activation. The Lck, Prkcb and Cd28 genes in the gene network were of high value, indicating an important relationship with protein synthesis and biological functions, the core node of the protein-protein network, and a high predictive ability of Lck and Cd28. CONCLUSIONS: The high-fat diet can induce changes in prostate tissue genes, leading to tumorigenesis.


Assuntos
Dieta Hiperlipídica , Próstata , Animais , Dieta Hiperlipídica/efeitos adversos , Redes Reguladoras de Genes , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Transcriptoma
2.
Am J Mens Health ; 15(4): 15579883211036786, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34330182

RESUMO

The objective of this study is to provide comprehensive and up-to-date estimates on the disease burden of BPH in 204 countries and territories between 1990 and 2019. Data about incidence, year lived with disability (YLD), and their age-standardized rates (ASRs) for 21 regions, 5 Socio-demographic Index (SDI) quintiles, 204 countries and territories, and 12 age categories from 1990 to 2019 were obtained from the Global Burden of Disease 2019 study. Estimated annual percentage changes (EAPCs) of the ASRs and the associations between SDI and the ASRs were estimated. The effects of population growth, population aging, and age-specific rate on the changes in the absolute numbers of incidence and YLD were quantified. Globally, there were 11.26 million (95% uncertainty interval [UI]: 8.79, 14.46) new cases and 1.86 million (95%UI: 1.13, 2.78) YLD due to BPH in 2019. The global ASRs of incidence (EAPC: -0.031, 95% CI: -0.050, -0.012) and YLD (EAPC: -0.058, 95% CI: -0.084, -0.031) decreased slightly from 1990 to 2019, whereas the absolute numbers increased dramatically from 1990 (incidence by 105.7% and YLD by 110.6%), mainly driven by the population growth (53.5% for incidence and 54.4% for YLD) and population aging (55.7% for incidence and 63.2% for YLD). The burden of BPH varied markedly among different regions, socioeconomic status, and countries. As the population is growing and aging, great efforts are required to develop effective prevention, treatment and management strategies to meet the high and increasing burden of BPH worldwide.


Assuntos
Pessoas com Deficiência/estatística & dados numéricos , Carga Global da Doença/estatística & dados numéricos , Hiperplasia Prostática/epidemiologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Humanos , Incidência , Expectativa de Vida , Masculino , Pessoa de Meia-Idade , Prevalência , Anos de Vida Ajustados por Qualidade de Vida , Fatores Socioeconômicos
3.
Zhonghua Nan Ke Xue ; 25(2): 103-109, 2019 Feb.
Artigo em Chinês | MEDLINE | ID: mdl-32216194

RESUMO

OBJECTIVE: To analyze the biological network regulation and key proteins of gene expression microarray in human normal prostate epithelial cells after treated with low-dose cadmium, and provide some new theoretical evidence for the pathogenesis of cadmium-related prostate cancer. METHODS: We downloaded 19 copies of gene chip data from the Gene Expression Omnibus (GEO), involving 9 samples of prostate epithelial cells exposed to low-dose cadmium and 10 cases of normal control. Using the Gene-Cloud of Biotechnology Informs platform, GenClip2.0 and Sytoscape 3.5.1, we screened differentially expressed genes, explored their protein interaction networks and biological pathways and, from the perspective of transcriptome, analyzed the changes in the genetic network of normal human prostate epithelial cells and their possible molecular biological functions after low-dose cadmium treatment. RESULTS: Totally, 1 050 (1.92%) differentially expressed genes were found in the prostate epithelial cells treated with low-dose cadmium, involved in such biological functions as the cell physiological process, MAPK regulation, regulation of intracellular signal transduction, and immunological effect. The HSP90AB1, BUB3 and PRKAR1A genes were the core nodes of the protein network, which showed statistically significant differences in their expressions and a correlation with the malignant transformation of normal cells. CONCLUSIONS: Low-dose cadmium can cause genetic changes in normal human prostate epithelial cells and the differentially expressed genes are mainly involved in such biological functions as the cell physiological process, MAPK regulation, regulation of intracellular signal transduction, and immunological effect.


Assuntos
Cádmio/efeitos adversos , Biologia Computacional , Células Epiteliais/metabolismo , Próstata/citologia , Transcriptoma , Proteínas de Ciclo Celular/metabolismo , Subunidade RIalfa da Proteína Quinase Dependente de AMP Cíclico/metabolismo , Células Epiteliais/efeitos dos fármacos , Perfilação da Expressão Gênica , Regulação Neoplásica da Expressão Gênica , Redes Reguladoras de Genes , Proteínas de Choque Térmico HSP90/metabolismo , Humanos , Masculino , Proteínas de Ligação a Poli-ADP-Ribose/metabolismo
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