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Microarray upon Sp110 knockdown in HepG2.2.15 cells

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE119072 | GEO | 2019/08/24

REPOSITORIES: GEO

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Project description:Hepatitis B virus (HBV) causes both acute and chronic liver inflammation. Approximately 600,000 CHB patients each year die of HBV-related diseases such as cirrhosis and liver cancer. Therefore, CHB remains a global health concern. Although there have been anti-HBV agents for treating CHB, they have some limitations including viral-drug resistance and adverse effects. Type III IFN or IFN-λ is promising to use as anti-HBV agents because of its anti-viral activities like type I IFNs. In addition, the expression of its receptor, IFNLR1, is limited only in epithelial cells including hepatocytes. Thus, treatment with IFN-lambda results in less side effects compared to IFN-alpha treatment. IFN-lambdas have been shown to inhibit the replication of several viruses including IAV, DENV, EMCV, HIV, HCV, and HBV; however, there have been no studies on the effects of IFN-λ3, the highest activity among other subtypes, on HBV replication. Therefore, this study aims to determine antiviral activities of IFN-λ3 against HBV replication and to investigate its molecular mechanism responsible for suppressing HBV propagation. The results showed that HBV transcripts and amount of intracellular HBV DNA were decreased in HepG2.2.15 cells, stable HBV-transfected hepatoblastoma cell line, treated with IFN-λ3 in a dose-dependent manner. This indicated that IFN-λ3 could inhibit HBV replication. Next, we performed quantitative proteomics to investigate the proteome changes in HepG2.2.15 treated with IFN-λ3. The proteins that changed their expressions were involved in several biological processes such as defense to viral infection, immune responses, cell-cell adhesion, transcription, translation, and metabolism. We further confirmed the proteomics results by immunoblotting assay. Consistent with MS data, it found that the expression of OAS3, SAMHD1 and STAT1 were increased as a result of IFN-λ3 stimulation. These results indicated that proteomics results were reproducible and reliable. Finally, we proposed 3 possible mechanisms involved in suppressing HBV replication including i.) IFN-λ3 induced anti-viral proteins affecting many steps in HBV life cycle ii.) IFN-λ3 promoted antigen processing and antigen presentation and iii.) IFN-λ3 rescued RIG-I signaling to promote both type I and type III IFN production.

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Microarray upon Sp110 knockdown in HepG2.2.15 cells

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