Evidence map›Paper›PMID 23056571›Full record

ArticlePloS one2012

Comparison of the regulation of β-catenin signaling by type I, type II and type III interferons in hepatocellular carcinoma cells.

Wei Li, Xiaojie Huang, Hongfei Tong, Yuxuan Wang, Tong Zhang, Wen Wang, Lili Dai, Tongzeng Li, Shengzhang Lin, Hao Wu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

15 citing papers in PubMed, 59 citations in OpenAlex.

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  11. Oncotarget · 2018
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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

10 authors at 5 institutions in 2 countries.

Wei LiDepartment of Infectious Diseases, Beijing You'an Hospital, Capital Medical University, China.
Xiaojie Huang
Hongfei Tong
Yuxuan Wang
Tong Zhang
Wen Wang
Lili Dai
Tongzeng Li
Shengzhang Lin
Hao Wu
Beijing YouAn Hospital · CNBinghamton University · USCapital Medical University · CNFirst Affiliated Hospital Zhejiang University · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectiveIFNs are a group of cytokines that possess potent antiviral and antitumor activities, while β-catenin pathway is a proliferative pathway involved in carcinogenesis. Interaction between these two pathways has not been well elaborated in hepatocellular carcinoma (HCC).

methodsHCC cell lines, HepG2 and Huh7, were used in this study. β-catenin protein levels and corresponding signaling activities were observed by flow cytometry and luciferase assay, respectively. Cell proliferation was quantified by counting viable cells under microscope, and apoptosis by TUNEL assay. DKK1 and GSK3β levels were determined by flow cytometry. Secreted DKK1 was tested by ELISA. FLUD, S3I and aDKK1 were used to inhibit STAT1, STAT3 and DKK1 activities, respectively.

resultsOur findings show that all three types of IFNs, IFNα, IFNγ and IFNλ, are capable of inhibiting β-catenin signaling activity in HepG2 and Huh7 cells, where IFNγ was the strongest (p<0.05). They expressed suppression of cellular proliferation and induced apoptosis. IFNγ expressed greater induction ability when compared to IFNα and IFNλ (p<0.05). All tested IFNs could induce DKK1 activation but not GSK3β in HepG2 and Huh7 cells. IFNs induced STAT1 and STAT3 activation but by using specific inhibitors, we found that only STAT3 is vital for IFN-induced DKK1 activation and apoptosis. In addition, DKK1 inhibitor blocked IFN-induced apoptosis. The pattern of STAT3 activation by different IFNs is found consistent with the levels of apoptosis with the corresponding IFNs (p<0.05).

conclusionsIn hepatocellular carcinoma, all three types of IFNs are found to induce apoptosis by inhibiting β-catenin signaling pathway via a STAT3- and DKK1-dependent pathway. This finding points to a cross-talk between different IFN types and β-catenin signaling pathways which might be carrying a biological effect not only on HCC, but also on processes where the two pathways bridge.

Indexed as

Apoptosisbeta CateninCarcinoma, HepatocellularCell Line, TumorCell ProliferationEnzyme-Linked Immunosorbent AssayFlow CytometryHep G2 CellsHumansIn Situ Nick-End LabelingIntercellular Signaling Peptides and ProteinsInterferon-gammaInterferonsInterferon Type ISignal TransductionSTAT1 Transcription Factorbeta CateninDKK1 protein, humanIntercellular Signaling Peptides and ProteinsInterferon-gammaInterferonsInterferon Type ISTAT1 Transcription FactorSTAT3 Transcription Factor

Identifiers

PMID23056571
PMCPMC3464253
OpenAlexW1967863535

What OpenQuestion holds

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LicenceCC BY
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.