Evidence map›Paper›PMID 19605487›Full record

ArticleJournal of virology2009

Hepatitis C virus core protein and cellular protein HAX-1 promote 5-fluorouracil-mediated hepatocyte growth inhibition.

Arup Banerjee, Kousuke Saito, Keith Meyer, Sutapa Banerjee, Malika Ait-Goughoulte, Ratna B Ray, Ranjit Ray

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Intrinsically disordered HAX-1 regulates CaBiochimica et biophysica acta. Biomembranes · 2020
    Article
  7. Article
  8. Article
  9. Article
  10. High expression of HAX-1 protein is associated with tumor growth in papillary thyroid carcinoma.International journal of clinical and experimental pathology · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. HAX-1 is overexpressed in hepatocellular carcinoma and promotes cell proliferation.International journal of clinical and experimental pathology · 2015
    Article
  15. Article
  16. Article
  17. Expression of HAX-1 in human colorectal cancer and its clinical significance.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  18. Article
  19. Article
  20. Article
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

7 authors at 1 institution in 1 country.

Arup BanerjeeDepartment of Internal Medicine, Saint Louis University, St. Louis, Missouri 63119, USA.
Kousuke Saito
Keith Meyer
Sutapa Banerjee
Malika Ait-Goughoulte
Ratna B Ray
Ranjit Ray
Saint Louis University · US

Funding

Mechanisms of Liver Disease Progression by Hepatitis C VirusR01DK080812 · NIDDK · SAINT LOUIS UNIVERSITY · PI RAY, RANJIT · 2009 to 2013
$1.6M
NIDDK NIH HHS DK080812NIDDK NIH HHS R01 DK080812
6 · The paper itself

Abstract

Hepatitis C virus (HCV) often causes chronic infection and may lead to hepatocellular carcinoma (HCC). We have shown previously that HCV core protein has pleiotropic functions, including transcriptional regulation of a number of cellular genes, although the mechanism for gene regulation remains unclear. In this study, a mammalian two-hybrid screen identified a novel binding partner, HS1-associated protein X-1 (HAX-1), for HCV core protein from a human liver cDNA library. An association between HAX-1 and HCV core protein was further verified by confocal microscopy and coimmunoprecipitation in HepG2 cells expressing HCV core or full-length (FL) gene. Both HCV core protein and a chemotherapeutic agent for HCC, 5-flouorouracil (5-FU), are known to modulate p53. We examined here whether an association between core and HAX-1 has any functional relevance to p53 modulation in 5-FU-treated cells. For this, the role of HAX-1 on 5-FU treatment was examined in HepG2 cells expressing HCV core or FL gene using cell proliferation, p53 expression, and caspase activation analysis. Cells expressing HCV-core or FL gene were more susceptible to 5-FU-induced growth inhibition than control cells, whereas cell survival was enhanced after suppression of HAX-1 by small interfering RNA. Further, 5-FU-mediated p53 expression was reduced with concurrent HAX-1 suppression in core- or polyprotein-expressing cells compared to control HepG2 cells, and caspase-2 and -7 activities were diminished. On the other hand, HCV core protein did not play a detectable role in 5-FU-mediated caspase-7 activation in the absence of functional p53 in Hep3B or Huh-7 cells. These observations underscore an association between HCV core and HAX-1, which promotes 5-FU mediated p53-dependent caspase-7 activation and hepatocyte growth inhibition.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntimetabolites, AntineoplasticCaspase 7Cell Line, TumorCell ProliferationChlorocebus aethiopsCOS CellsDNA, ComplementaryEnzyme ActivationFluorouracilHepatocytesHumansMicroscopy, ConfocalProteinsViral Core ProteinsAdaptor Proteins, Signal TransducingAntimetabolites, AntineoplasticCaspase 7DNA, ComplementaryFluorouracilHAX1 protein, humannucleocapsid protein, Hepatitis C virusProteinsViral Core Proteins

Identifiers

PMID19605487
PMCPMC2748019
OpenAlexW2130040347

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.