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Obesity synergizes with HBx, Src and p53 mutation accelerate hepatocarcinogenesis

ABSTRACT: Obesity synergizes with HBx, Src and p53 mutation accelerate hepatocarcinogenesis

PROVIDER: PRJNA555327 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9707990_1.fastq.gz	Fastqsanger.gz
	SRR9707990_2.fastq.gz	Fastqsanger.gz
	SRR9708000_1.fastq.gz	Fastqsanger.gz
	SRR9708000_2.fastq.gz	Fastqsanger.gz
	SRR9707991_1.fastq.gz	Fastqsanger.gz

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Obesity synergizes with HBx, Src and p53 mutation accelerate hepatocarcinogenesis [Microarray]

Project description:Obesity synergizes with HBx, Src and p53 mutation accelerate hepatocarcinogenesis [Microarray]

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Obesity synergizes with HBx, Src and p53 mutation accelerate hepatocarcinogenesis [RNA-seq]

Project description:Obesity synergizes with HBx, Src and p53 mutation accelerate hepatocarcinogenesis [RNA-seq]

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Obesity synergizes with HBx, Src and p53 mutation accelerate hepatocarcinogenesis [Microarray]

Project description:Previous studies have identified liver cancer associated to NASH, diabetes, obesity, and some genetic risk factors. We want to investigate the synergism between diet and genetic risk factors in hepatocarcinogenesis using omics data of four background zebrafish in three types of diet. We found the fishes have more genetic risk factors at the same time, and have higher probability to accelerate cancer formation. Overfed and high fat diet will increase the chance. Moreover, the results showed metabolism and genetic information processing, including the pathways of fatty acid metabolism, steroid biosynthesis and ribosome biogenesis are highly affected in hepatocellular carcinoma.

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Obesity synergizes with HBx, Src and p53 mutation accelerate hepatocarcinogenesis [RNA-seq]

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Obesity synergizes with HBx, Src and p53 mutation accelerate hepatocarcinogenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-07-19 | GSE134496 | GEO

Gene Expression Analysis for HBx-induced HCC Mouse Model

Project description:Hepatoarcinogenesis is a slow and multistep process. We used Hepatitis B virus X antigen (HBx) induced Hepatocellular carcinoma (HCC) as model. We also identify the biomarkers, the pathways and networks underlying HCC formation in this animal model. We analyzed the events from the early, middle, and late stages, in order to predict and prevent the development of cancer. At each specific stage, we analyzed the expression level that differed at least two-fold between HBx transgenic and wild-type mouse liver. Statistical approaches were used to identify genes displaying an increasing or decreasing trend throughout hepatocarcinogenesis. The liver was excised from 6-week-, 8-month-, 12-month-, 14-month-, and 16-month-old HBx transgenic mice (A106 strain) and RNA samples were isolated. In both 14-month- and 16-month-old mice, samples were obtained from both the tumor tissue and the normal.

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LncRNAs expression profiles in the livers of 20-month-old male HBx transgenic mice and C57BL/6 wild-type mice

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Expression data from adult transgenic zebrafish

Project description:Hepatocellular carcinoma is the fourth leading cause of cancer-related deaths worldwide. Many carcinogens induce inflammation and cirrhosis, and eventually develop into liver cancer. Fucoidan is sulfated polysaccharide that is mainly found in brown seaweeds. In this study, we investigated the effects and mechanisms of low molecular weight fucoidan (i.e. oligo-fucoidan) preventing hepatocarcinogenesis using HBx,Src, and HBx,Src,p53-/+ transgenic zebrafish liver cancer model. Using an oligo-fucoidan oral gavage in adult transgenic zebrafish, we then used microarrays to detail the global programme of gene expression after fucoidan treatment and identified distinct classes of up- and down-regulated genes during this process.

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Project description:The hepatitis B virus X protein (HBx) has been implicated as an oncogene in both epigenetic modifications and genetic regulation during hepatocarcinogenesis, but the underlying mechanisms are not entirely clear. Long non-coding RNAs (lncRNAs), which regulate gene expression with little or no protein-coding capacity, are involved in diverse biological processes and in carcinogenesis. We asked whether HBx could promote hepatocellular carcinoma (HCC) by regulating the expression of lncRNAs.In this study, we investigated the alteration in expression of lncRNAs induced by HBx using microarrays, and our results indicate that HBx transgenic mice have a specific profile of liver lncRNAs compared with wild-type mice. For these experiments, six each of 20-month-old male HBx-transgenic mice and wild-type C57BL/6 mice were sacrificed and the livers were removed. Every three livers were pooled as one sample; therefore, each group was represented by two samples. The total RNA was extracted from the four samples and used for microarray experiments. Mouse LncRNA Array (4 x 44K, ArrayStar, Rockville, MD) were used to monitor the expression level of approximately 14000 lncRNAs identified from the NCBI RefSeq, UCSC, RNAdb2.0, NRED, Fantom3.0 and UCRs. LncRNAs differentially expressed were identified by comparing expression levels in HBx-transgenic mice and wild-type mice.

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