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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: Not available

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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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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.

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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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