Evidence map›Paper›PMID 24240095›Full record

ArticleThe Journal of biological chemistry2013

Mechanism of hepatitis C virus (HCV)-induced osteopontin and its role in epithelial to mesenchymal transition of hepatocytes.

Jawed Iqbal, Steven McRae, Krishna Banaudha, Thi Mai, Gulam Waris

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Article
  3. Impact of osteopontin on the development of non-alcoholic liver disease and related hepatocellular carcinoma.Liver international : official journal of the International Association for the Study of the Liver · 2020
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  12. Review
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  14. Observational
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Jawed IqbalFrom the Department of Microbiology and Immunology, H. M. Bligh Cancer Research Laboratories, Rosalind Franklin University of Medicine and Science, Chicago Medical School, North Chicago, Illinois 60064 and.
Steven McRae
Krishna Banaudha
Thi Mai
Gulam Waris
Rosalind Franklin University of Medicine and Science · USGeorge Washington University · US

Funding

Role of the inflammasome in hepatitis C virus pathogenesisR56AI089772 · NIAID · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · PI WARIS, GULAM · 2012 to 2012
$386k
NIAID NIH HHS 1R56AI089772-01A1NIAID NIH HHS R56 AI089772
6 · The paper itself

Abstract

Osteopontin (OPN) is a secreted phosphoprotein, originally characterized in malignant-transformed epithelial cells. OPN is associated with tumor metastasis of several tumors and is overexpressed in hepatocellular carcinoma (HCC) tissue involving HCC invasion and metastasis. Importantly, OPN is significantly up-regulated in liver injury, inflammation, and hepatitis C virus (HCV)-associated HCC. However, the underlying mechanisms of OPN activation and its role in HCV-mediated liver disease pathogenesis are not known. In this study, we investigated the mechanism of OPN activation in HCV-infected cells. We demonstrate that HCV-mediated Ca(2+) signaling, elevation of reactive oxygen species, and activation of cellular kinases such as p38 MAPK, JNK, PI3K, and MEK1/2 are involved in OPN activation. Incubation of HCV-infected cells with the inhibitors of AP-1 and Sp1 and site-directed mutagenesis of AP-1- and Sp1-binding sites on the OPN promoter suggest the critical role of AP-1 and Sp1 in OPN promoter activation. In addition, we show the in vivo interactions of AP-1 and Sp1 with the OPN promoter using chromatin immunoprecipitation assay. We also show the calpain-mediated processing of precursor OPN (∼75 kDa) into ∼55-, ∼42-, and ∼36-kDa forms of OPN in HCV-infected cells. Furthermore, we demonstrate the critical role of HCV-induced OPN in increased phosphorylation of Akt and GSK-3β followed by the activation of β-catenin, which can lead to EMT of hepatocytes. Taken together, these studies provide an insight into the mechanisms of OPN activation that is relevant to the metastasis of HCV-associated HCC.

Indexed as

Epithelial-Mesenchymal Transitionbeta CateninCalcium SignalingCalpainCarcinoma, HepatocellularCell Line, TumorExtracellular Signal-Regulated MAP KinasesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHepacivirusHepatitis CHepatocytesHumansLiver NeoplasmsNeoplasm MetastasisOsteopontinbeta CateninCalpainExtracellular Signal-Regulated MAP KinasesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanOsteopontinProto-Oncogene Proteins c-aktSp1 Transcription FactorTranscription Factor AP-1Epithelial Mesenchymal TransitionHepatitis C VirusMetastasisOsteopontinOxidative Stress

Identifiers

PMID24240095
PMCPMC3873557
OpenAlexW1996327054

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.