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Title: Gene expression profiling and network analysis reveals lipid and steroid metabolism to be the most favored by TNF? in HepG2 cells
Authors: Pandey A.K. 
Munjal N.
Datta M.
Keywords: actin related protein
aquaporin 3
CCAAT enhancer binding protein alpha
DDX54 protein
DNA methyltransferase 3B
E47 protein
fibroblast growth factor receptor 5
Freac 7 protein
heat shock protein 90
herpesvirus entry mediator
immunoglobulin E
immunoglobulin enhancer binding protein
immunoglobulin receptor
interferon regulatory factor 1
MEF 2 protein
protein p300
Ryk protein
SLC25A5 protein
sterol regulatory element binding protein 1
TBL1X protein
tissue inhibitor of metalloproteinase 1
transcription factor foxd3
transcription factor FOXJ2
transcription factor NF E2
tumor necrosis factor alpha
unclassified drug
unindexed drug
tumor necrosis factor alpha
binding site
cancer cell culture
down regulation
gene cluster
gene expression
gene expression profiling
human cell
human cell culture
immune response
lipid metabolism
liver cell
liver cell carcinoma
microarray analysis
nucleotide sequence
protein binding
steroid metabolism
cell strain HepG2
cluster analysis
DNA microarray
drug effect
gene expression regulation
gene regulatory network
reverse transcription polymerase chain reaction
Cluster Analysis
Gene Expression Profiling
Gene Expression Regulation, Neoplastic
Gene Regulatory Networks
Hep G2 Cells
Lipid Metabolism
Oligonucleotide Array Sequence Analysis
Reverse Transcriptase Polymerase Chain Reaction
Tumor Necrosis Factor-alpha
Issue Date: 2010
Citation: Pandey A.K., Munjal N., Datta M. (2010). Gene expression profiling and network analysis reveals lipid and steroid metabolism to be the most favored by TNF? in HepG2 cells. PLoS ONE 5 (2) : e9063. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
Abstract: Background:The proinflammatory cytokine, TNF?, is a crucial mediator of the pathogenesis of several diseases, more so in cases involving the liver wherein it is critical in maintaining liver homeostasis since it is a major determiner of hepatocyte life and death. Gene expression profiling serves as an appropriate strategy to unravel the underlying signatures to envisage such varied responses and considering this, gene transcription profiling was examined in control and TNF? treated HepG2 cells. Methods and Findings:Microarray experiments between control and TNF? treated HepG2 cells indicated that TNF? could significantly alter the expression profiling of 140 genes; among those up-regulated, several GO (Gene Ontology) terms related to lipid and fat metabolism were significantly (p<.01) overrepresented indicating a global preference of fat metabolism within the hepatocyte and those within the down-regulated dataset included genes involved in several aspects of the immune response like immunoglobulin receptor activity and IgE binding thereby indicating a compromise in the immune defense mechanism(s). Conserved transcription factor binding sites were identified in identically clustered genes within a common GO term and SREBP-1 and FOXJ2 depicted increased occupation of their respective binding elements in the presence of TNF?. The interacting network of "lipid metabolism, small molecule biochemistry" was derived to be significantly overrepresented that correlated well with the top canonical pathway of "biosynthesis of steroids". Conclusions:TNF? alters the transcriptome profiling within HepG2 cells with an interesting catalog of genes being affected and those involved in lipid and steroid metabolism to be the most favored. This study represents a composite analysis of the effects of TNF? in HepG2 cells that encompasses the altered transcriptome profiling, the functional analysis of the up- and down- regulated genes and the identification of conserved transcription factor binding sites. These could possibly determine TNF? mediated alterations mainly the phenotypes of hepatic steatosis and fatty liver associated with several hepatic pathological states. � 2010 Pandey et al.
Source Title: PLoS ONE
ISSN: 19326203
DOI: 10.1371/journal.pone.0009063
Rights: Attribution 4.0 International
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