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Genome-wide Transcriptome Analysis of CD36 Overexpression in HepG2.2.15 Cells to Explore Its Regulation Role of Metabolism and HBV Life Cycle

ABSTRACT: To understand the molecular basis underlying the response to increasing CD36 overexpression in HepG2.2.15 cell, we performed genome-wide sequencing of the mRNAs from HepG2.2.15-CD36OE cell and HepG2.2.15-vector cell using the RNA-seq technology to detect its differential transcriptomic profile.

ORGANISM(S): Homo sapiens

PROVIDER: GSE83577 | GEO | 2017/01/01

SECONDARY ACCESSION(S): PRJNA326403

REPOSITORIES: GEO

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Genome-Wide Transcriptome Analysis of CD36 Overexpression in HepG2.2.15 Cells to Explore Its Regulatory Role in Metabolism and the Hepatitis B Virus Life Cycle.

Project description:Hepatitis B virus (HBV) is a hepatocyte-specific DNA virus whose gene expression and replication are closely associated with hepatic metabolic processes. Thus, a potential anti-viral strategy is to target the host metabolic factors necessary for HBV gene expression and replication. Recent studies revealed that fatty acid translocase CD36 is involved in the replication, assembly, storage, and secretion of certain viruses, such as hepatitis C virus (HCV) and human immunodeficiency virus (HIV). However, the relationship between CD36 and the HBV life cycle remains unclear. Here, we showed, for the first time, that increased CD36 expression enhances HBV replication in HepG2.2.15 cells. To understand the underlying molecular basis, we performed genome-wide sequencing of the mRNA from HepG2.2.15-CD36 overexpression (CD36OE) cells and HepG2.2.15-vector cells using RNA Sequencing (RNA-seq) technology to analyze the differential transcriptomic profile. Our results identified 141 differentially expressed genes (DEGs) related to CD36 overexpression, including 79 upregulated genes and 62 downregulated genes. Gene ontology and KEGG pathway analysis revealed that some of the DEGs were involved in various metabolic processes and the HBV life cycle. The reliability of the RNA-Seq data was confirmed by qPCR analysis. Our findings provide clues to build a link between CD36, host metabolism and the HBV life cycle and identified areas that require further investigation.

| S-EPMC5066966 | biostudies-literature

Differentially expressed miRNAs between HepG2.2.15 and HepG2 cells

Project description:MiRNAs are important posttranscriptional regulators in various physiological processes and their dysregulations have been found in diseases such as infection, imflammation and cancer. Here we compared the miRNA profilings between HBV-producing HepG2.2.15 and its non-HBV maternal HepG2 cell to find potential miRNAs involving in HBV expression. The result indicated that some of the deregulated miRNAs in HepG2.2.15 have been implicated in viral infection and the processes of the immune regulation. HepG2.2.15 vs. HepG2

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CD36 deficiency inhibits proliferation by cell cycle control in skeletal muscle cells

Project description:Obesity-related muscular dysfunction and relative muscle atrophy affect an increasing number of people. Elucidating the molecular mechanisms of skeletal muscle cell development and growth may contribute to the maintenance of skeletal muscle mass in obesity. Fatty acid translocase (FAT/CD36), as a long-chain fatty acid transport protein, is crucial for lipid metabolism and signaling. CD36 is known to function in myogenic differentiation, and whether it affects the proliferation of skeletal muscle cells and the underlying mechanisms remain unclear. In this study, the effect of CD36 deficiency on skeletal muscle cell viability and proliferation was examined using C2C12 myoblasts. Results showed that the deletion of CD36 enhanced the inhibitory effect of PA on the proliferation and the promotion of apoptosis in skeletal muscle cells. Intriguingly, the silencing of CD36 suppressed cell proliferation by preventing the cell cycle from the G0/G1 phase to the S phase in a cyclin D1/CDK4-dependent manner. Overall, we demonstrated that CD36 was involved in skeletal muscle cell proliferation by cell cycle control, and these findings might facilitate the treatment of obesity-related muscle wasting.

2022-05-27 | GSE204686 | GEO

Gene-expression profiles of HepG2.2.15 cells induced by overexpression of Complement 2

Project description:To explore the effect of overexpression of complement component 2 (C2) on HepG2.2.15 cells, we established HepG2.2.15-mock cells and C2-overexpressing HepG2.2.15 cells (HepG2.2.15-shC2) to identify differentially expressed genes and then performed GO and KEGG analysis to identified the altered pathways caused by over-expression of C2.

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Microarray upon Sp110 knockdown in HepG2.2.15 cells

Project description:Hepatitis B virus (HBV), belonging to Hepadnaviridae family, remains undetected in early infection and is known to be the cause of several hepatic diseases leading to cirrhosis and hepatocellular carcinoma. We have found that PML-Nuclear Body Speckled 110kDa (Sp110), is hyper-expressed upon HBV infection and intriguingly, Sp110 knock-down significantly reduced viral DNA-load in the culture supernatant of HepG2.2.15 (a HBV expressing cell-line). To understand the molecular basis underlying the viral elimination upon Sp110 silencing in HepG2.2.15 cells, we performed microarray to find the differential transcriptomics in Control siRNA treated vs. Sp110 siRNA treated cells. To understand the molecular basis underlying the viral elimination upon Sp110 silencing in HepG2.2.15 cells, we performed microarray to find the differential transcriptomics in Control siRNA treated vs. Sp110 siRNA treated cells.

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Differentially expressed miRNAs between HepG2.2.15 and HepG2 cells

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mRNA sequencing of ADH4 overexpression in HBV-associated hepatoma cell line HepG2.2.15

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AMSC CD36+ subpopulations

Project description:Adipose-derived MSCs (AMSC) are currently utilized in clinical trials for various diseases including osteoarthritis, amyotrophic lateral sclerosis, and multiple system atrophy. Whilst AMSCs may be defined by the surface expression of classical markers including CD44, CD90, CD105, and absence of CD45, these cells may exhbit donor-to-donor differences in differentiation potential. In this study we evaluated the expression of CD36 amongst AMSCs and utilized magnetic cell sorting to enrich for CD36+ cells. Whole transcriptome RNA-sequencing was performed on unsorted, CD36+ enriched, and CD36+ depleted cells to determine gene expression difference between these populations of cells. CD36 sorted or unsorted cells were then plated and maintained in growth medium. Cells were expanded for 2 passages and passage 8 cells were plated for RNA-sequencing analysis. Trizol reagent was used to harvest cells when they were proliferating cells (~80%) or 100% confluent cells.

2021-11-28 | GSE189525 | GEO

AMSC CD36+ subpopulations

Project description:AMSC CD36+ subpopulations

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HBV Integration-mediated Cell Apoptosis in HepG2.2.15.

Project description:Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer and the second leading cause of cancer deaths in the word. Hepatitis B virus (HBV) infection plays an important role in the development of HCC. However, the mechanisms by which HBV integration affects host cells remain poorly understood. HepG2.2.15 cell line is derived from HCC cell line HepG2 with stable transfection HBV expression. In this study, HepG2.2.15 cells showed decreased proliferation, G1 cell cycle arrest and increased apoptosis, when compared to HepG2 cells. HBV capture sequencing was conducted in both genome and transcriptome level, followed by RNA expression sequencing in HepG2.2.15. Here, CAMSAP2/CCDC12/DPP7/OR4F3 were found to be targets for HBV integration in both genome and transcriptome level, accompanied by alteration in their expression when compared to HepG2. Among these genes, DPP7 was the only one gene with HBV integration into its exon, meanwhile DPP7 expression level was also downregulated in HepG2.2.15 as compared to HepG2. Furthermore, DPP7 knockdown resulted in increased apoptosis through upregulation of the Bax/Bcl2 ratio in HepG2 cells. Our results suggest that HBV integration of DPP7 was involved in cell apoptosis.

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