Evidence map›Paper›PMID 25501304›Full record

ArticleInternational journal of cancer2015

Inhibition of mesothelioma cancer stem-like cells with adenovirus-mediated NK4 gene therapy.

Xu-Bin Deng, Li Xiao, Yue Wu, Fang Jin, Brooke Mossman, Joseph R Testa, Guang-Hui Xiao

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Antiproliferation activities of NK4 on multiple myeloma.Experimental and therapeutic medicine · 2018
    Article
  9. The role of MALAT1/miR-1/slug axis on radioresistance in nasopharyngeal carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    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 3 institutions in 2 countries.

Xu-Bin DengCancer Institute, Southern Medical University, Guangzhou, China.
Li XiaoCancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA.
Yue WuCancer Institute, Southern Medical University, Guangzhou, China.
Fang JinCancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA.
Brooke MossmanDepartment of Pathology, University of Vermont College of Medicine, Burlington, VT.
Joseph R TestaCancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA.
Guang-Hui XiaoCancer Institute, Southern Medical University, Guangzhou, China.
Fox Chase Cancer Center · USZero to Three · USUniversity of Vermont · US

Funding

Translational Research Support CoreP30ES013508 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI Rebecca A Simmons · 2006 to 2026
$35.3M
PATHOLOGY, VIROLOGY, AND ANIMAL COREP01CA114047 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI TESTA, JOSEPH R. · 2006 to 2010
$8.0M
NCI NIH HHS CA-114047NCI NIH HHS P01 CA114047NIEHS NIH HHS P30 ES013508
6 · The paper itself

Abstract

Malignant mesothelioma (MM) is a highly invasive and chemoresistant malignancy induced by asbestos fibers. NK4, a hepatocyte growth factor antagonist and angiogenesis inhibitor, consists of the N-terminal hairpin domain and four kringle domains of the α-chain of hepatocyte growth factor. The therapeutic potential of NK4 has been demonstrated in a variety of tumor types. However, the mechanisms by which NK4 inhibits tumor growth have not been well delineated. In this study, it is shown that the NK4 adenovirus (Ad-NK4) potently inhibits cell viability, invasiveness and tumorigenicity of human MM cells. Significantly, this study demonstrates for the first time that Ad-NK4 inhibits cancer stem-like cell (CSC) properties as assessed by spheroid formation assay, side population analysis and flow cytometric sorting of CD24 cells. In addition to inhibiting phosphorylation of Met and AKT, Ad-NK4 markedly suppressed the active form of β-catenin, a key mediator of both Wnt and AKT pathways. It is further demonstrated that expression of NK4 suppresses β-catenin nuclear localization and transcriptional activity. Intriguingly, the expression levels of Oct4 and Myc, two critical stem cell factors and downstream targets of β-catenin, were also diminished by Ad-NK4. Furthermore, the strong antitumor effect of NK4 was found to be linked to its ability to inhibit CSCs as revealed by immunohistochemical examination of tumor specimens from a mouse xenograft model of human MM. These findings suggest that NK4 acts as a CSC inhibitor by impeding Met/AKT/β-catenin signaling and holds promise for achieving durable therapeutic responses in MM by constraining the CSC component of these aggressive tumors.

Indexed as

AdenoviridaeAnimalsbeta CateninBlotting, WesternCell Line, TumorCell SurvivalGenetic TherapyGenetic VectorsHepatocyte Growth FactorHumansIndolesLung NeoplasmsMesotheliomaMesothelioma, MalignantMice, NudeMicroscopy, Fluorescence5-((2,6-dichlorobenzyl)sulfonyl)-3-((3,5-dimethyl-4-((2-(pyrrolidin-1-ylmethyl)pyrrolidin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-1,3-dihydro-2H-indol-2-onebeta CateninHepatocyte Growth FactorHGF protein, humanIndolesProto-Oncogene Proteins c-metSulfonescancer stem-like cellsHGF/Metmalignant mesotheliomaNK4therapy

Identifiers

PMID25501304
PMCPMC4428975
OpenAlexW2139084407

What OpenQuestion holds

Textmetadata
LicenceTDM
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.