Evidence map›Paper›PMID 25726528›Full record

ArticleOncotarget2015

Adenovirus expressing dual c-Met-specific shRNA exhibits potent antitumor effect through autophagic cell death accompanied by senescence-like phenotypes in glioblastoma cells.

Jung-Sun Lee, Eonju Oh, Ji Young Yoo, Kyeong Sook Choi, Mi Jin Yoon, Chae-Ok Yun

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Why is Mortalin a Potential Therapeutic Target for Cancer?Frontiers in cell and developmental biology · 2022
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Increased Expression of c-Met is Associated with Chemotherapy-Resistant Breast Cancer and Poor Clinical Outcome.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  11. Article
  12. Article
  13. Hepatoma targeting peptide conjugated bio-reducible polymer complexed with oncolytic adenovirus for cancer gene therapy.Journal of controlled release : official journal of the Controlled Release Society · 2015
    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

6 authors at 3 institutions in 1 country.

Jung-Sun LeeInstitute for Cancer Research, Yonsei University College of Medicine, Seoul, Korea.
Eonju OhDepartment of Bioengineering, College of Engineering, Hanyang University, Seoul, Korea.
Ji Young YooInstitute for Cancer Research, Yonsei University College of Medicine, Seoul, Korea.
Kyeong Sook ChoiDepartment of Molecular Science & Technology, Institute for Medical Sciences, Ajou University School of Medicine, Suwon, Korea.
Mi Jin YoonDepartment of Molecular Science & Technology, Institute for Medical Sciences, Ajou University School of Medicine, Suwon, Korea.
Chae-Ok YunDepartment of Bioengineering, College of Engineering, Hanyang University, Seoul, Korea.
Ajou University · KRHanyang University · KRYonsei University · KR

Funding

RGD-POLYMER TARGETING PLASMID TO ANGIOGENIC ENDOTHELIUMR01CA107070 · NCI · UNIVERSITY OF UTAH · PI KIM, SUNG WAN · 2004 to 2013
$2.7M
NCI NIH HHS CA 107070NCI NIH HHS R01 CA107070
6 · The paper itself

Abstract

c-Met, a cognate receptor tyrosine kinase of hepatocyte growth factor, is overexpressed and/or mutated in number of tumors. Therefore, abrogation of c-Met signaling may serve as potential therapeutic targets. In this study, we generated Ads expressing single shRNA specific to c-Met (shMet) (dl/shMet4 and dl/shMet5) or dual shRNAs specific to c-Met (dl/shMet4+5); and examined the therapeutic potential of these newly engineered Ads in targeting c-Met, and delineated their mechanism of action in vitro and in vivo. Ads expressing shMet induced knock-down in c-Met, and phenotypically resulted in autophagy-like features including appearance of membranousvacuoles, formation of acidic vesicular organelles, and cleavage and recruitment of microtubule-associated protein1 light chain 3 to autophagosomes. Ads expressing shMet also suppressed Akt phosphorylation and increased number of senescence-related gene products including SM22, TGase II, and PAI-1. These changes resulted in inhibition of cell proliferation and G2/M arrest of U343 cells. In vivo, intratumoral injection with dl/shMet4+5 resulted in a significant reduction of tumor growth with corresponding increasing overall survival. Histopathological analysis of these treated tumors revealed that Atg5 was highly up-regulated, indicating the therapeutic induction of autophagy. In sum, these results reveal that autophagic cell death induced by shMet-expressing Ads provide a novel strategy for targeting c-Met-expressing tumors through non-apoptotic mechanism of cell death.

Indexed as

AdenoviridaeAnimalsAutophagyBrain NeoplasmsCell Line, TumorGene Knockdown TechniquesGenetic TherapyGlioblastomaHumansMaleMiceMice, NudePhenotypeProto-Oncogene Proteins c-metRNA, Small InterferingSignal TransductionMET protein, humanProto-Oncogene Proteins c-metRNA, Small Interfering

Identifiers

PMID25726528
PMCPMC4414172
OpenAlexW1489818667

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.