Evidence map›Paper›PMID 20012654›Full record

ArticleJournal of gastroenterology2010

Comparison of HCV-associated gene expression and cell signaling pathways in cells with or without HCV replicon and in replicon-cured cells.

Yuki Nishimura-Sakurai, Naoya Sakamoto, Kaoru Mogushi, Satoshi Nagaie, Mina Nakagawa, Yasuhiro Itsui, Megumi Tasaka-Fujita, Yuko Onuki-Karakama, Goki Suda, Kako Mishima and 11 more

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Journal of gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Metabolic alterations and hepatitis C: From bench to bedside.World journal of gastroenterology · 2016
    Review
  6. Article
  7. Article
  8. Psammaplin A inhibits hepatitis C virus NS3 helicase.Journal of natural medicines · 2013
    Article
  9. CD133: a stem cell biomarker and beyond.Experimental hematology & oncology · 2013
    Article
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  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

21 authors.

Yuki Nishimura-SakuraiDepartment of Gastroenterology and Hepatology, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.
Naoya Sakamoto
Kaoru Mogushi
Satoshi Nagaie
Mina Nakagawa
Yasuhiro Itsui
Megumi Tasaka-Fujita
Yuko Onuki-Karakama
Goki Suda
Kako Mishima
Machi Yamamoto
Mayumi Ueyama
Yusuke Funaoka
Takako Watanabe
Seishin Azuma
Yuko Sekine-Osajima
Sei Kakinuma
Kiichiro Tsuchiya
Nobuyuki Enomoto
Hiroshi Tanaka
Mamoru Watanabe

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatitis C virus (HCV) replication is affected by several host factors. Here, we screened host genes and molecular pathways that are involved in HCV replication by comprehensive analyses using two genotypes of HCV replicon-expressing cells, their cured cells and naïve Huh7 cells.

methodsHuh7 cell lines that stably expressed HCV genotype 1b or 2a replicon were used. The cured cells were established by treating HCV replicon cells with interferon-alpha. Expression of 54,675 cellular genes was analyzed by GeneChip DNA microarray. The data were analyzed by using the KEGG Pathway database.

resultsHierarchical clustering analysis showed that the gene-expression profiles of each cell group constituted clear clusters of naïve, HCV replicon-expressed, and cured cell lines. The pathway process analysis between the replicon-expressing and the cured cell lines identified significantly altered pathways, including MAPK, steroid biosynthesis and TGF-beta signaling pathways, suggesting that these pathways were affected directly by HCV replication. Comparison of cured and naïve Huh7 cells identified pathways, including steroid biosynthesis and sphingolipid metabolism, suggesting that these pathways were required for efficient HCV replication. Cytoplasmic lipid droplets were obviously increased in replicon-expressing and cured cells as compared to naïve cells. HCV replication was significantly suppressed by peroxisome proliferator-activated receptor (PPAR)-alpha agonists but augmented by PPAR-gamma agonists.

conclusionComprehensive gene expression and pathway analyses show that lipid biosynthesis pathways are crucial to support proficient virus replication. These metabolic pathways could constitute novel antiviral targets against HCV.

Indexed as

Cell Culture TechniquesCell LineCluster AnalysisGene Expression ProfilingGenes, ViralHepacivirusHumansLipid MetabolismOligonucleotide Array Sequence AnalysisRepliconSignal TransductionVirus Replication

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.