eprintid: 10050639
rev_number: 22
eprint_status: archive
userid: 608
dir: disk0/10/05/06/39
datestamp: 2018-06-21 14:52:29
lastmod: 2021-09-18 21:49:27
status_changed: 2018-06-21 14:52:29
type: article
metadata_visibility: show
creators_name: Huang, J
creators_name: Zhao, L
creators_name: Yang, P
creators_name: Chen, Z
creators_name: Tang, N
creators_name: Ruan, XZ
creators_name: Chen, Y
title: 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
ispublished: pub
divisions: UCL
divisions: B02
divisions: C10
divisions: D17
divisions: G93
note: Copyright: © 2016 Huang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
abstract: 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.
date: 2016-10-17
date_type: published
publisher: PUBLIC LIBRARY SCIENCE
official_url: http://doi.org/10.1371/journal.pone.0164787
oa_status: green
full_text_type: pub
language: eng
primo: open
primo_central: open_green
verified: verified_manual
elements_id: 1194692
doi: 10.1371/journal.pone.0164787
lyricists_name: Ruan, Xiong-Zhong
lyricists_id: XZRUA13
actors_name: Henderson, Kathryn
actors_id: KJHEN38
actors_role: owner
full_text_status: public
publication: PLoS One
volume: 11
number: 10
article_number: e0164787
pages: 15
issn: 1932-6203
citation:        Huang, J;    Zhao, L;    Yang, P;    Chen, Z;    Tang, N;    Ruan, XZ;    Chen, Y;      (2016)    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.                   PLoS One , 11  (10)    , Article e0164787.  10.1371/journal.pone.0164787 <https://doi.org/10.1371/journal.pone.0164787>.       Green open access   
 
document_url: https://discovery.ucl.ac.uk/id/eprint/10050639/1/Genome-Wide%20Transcriptome%20Analysis%20of%20CD36%20Overexpression%20in%20HepG2.2.15%20Cells%20to%20Explore%20Its%20Regulatory%20Role%20in%20Metabolism%20and%20the%20Hepatitis%20B%20Virus%20Life%20Cycle.pdf