Evidence map›Paper›PMID 26208481›Full record

ArticleOncotarget2015

MDA5 complements TLR3 in suppression of neuroblastoma.

Wen-Ming Hsu, Chao-Cheng Huang, Hsin-Yu Lee, Pei-Yi Wu, Min-Tsui Wu, Hui-Ching Chuang, Li-Ling Lin, Jiin-Haur Chuang

Abstract 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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. The Involvement of CSRP1 in Neuroblastoma Differentiation and Apoptosis Impacting Tumor-Suppressive Therapeutic Responses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  5. CD68Frontiers in oncology · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Downregulation of c-Myc is involved in TLR3-mediated tumor death of neuroblastoma xenografts.Laboratory investigation; a journal of technical methods and pathology · 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

8 authors.

Wen-Ming HsuDepartment of Surgery, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.
Chao-Cheng HuangDepartment of Pathology, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Hsin-Yu LeeDepartment of Life Science and Institute of Zoology, National Taiwan University, Taipei, Taiwan.
Pei-Yi WuDepartment of Life Science and Institute of Zoology, National Taiwan University, Taipei, Taiwan.
Min-Tsui WuDepartment of Pediatric Surgery, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Hui-Ching ChuangDepartment of Otolaryngology, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Li-Ling LinDepartment of Pediatric Surgery, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Jiin-Haur ChuangDepartment of Pediatric Surgery, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptor3 (TLR3) has been confirmed to be differentially expressed in neuroblastoma (NB), and predicts a favorable prognosis with a high expression in tumor tissues. Treatment with TLR3 agonist--polyinosinic-polycytidylic acid [poly(I:C)] could induce significant but limited apoptosis in TLR3-expressing NB cells, suggesting that other viral RNA sensors, including melanoma differentiation-associated gene 5 (MDA5) and retinoic acid-inducible gene-I (RIG-I) in the cytosolic compartment might also be implicated in poly(I:C)-induced NB cell death. MDA5 and RIG-I were induced by poly(I:C) to express in two of six NB cell lines, SK-N-AS (AS) and SK-N-FI, which were associated with up-regulation of caspase9 and active caspase3. While knockdown of either MDA5 or RIG-I alone is ineffective to decrease caspase9 and active caspase3, simultaneously targeting MDA5 and TLR3 showed the best effect to rescue poly(I:C) induced up-regulation of mitochondrial antiviral signaling protein (MAVS), caspase9, active caspase3, and apoptosis in AS cells. Over-expression of MDA5 in FaDu cells resulted in significantly less colony formation and more poly(I:C)-induced cell death. Further studies in human NB tissue samples revealed that MDA5 expression in NB tissues predicted a favorable prognosis synergistically with TLR3. Our findings indicate that MDA5 may serve as a complementary role in the TLR3 activated suppression of NB.

Indexed as

ApoptosisBlotting, WesternCaspase 3Caspase 9ChildChild, PreschoolDEAD Box Protein 58DEAD-box RNA HelicasesFemaleGene Expression Regulation, NeoplasticHumansInfantInfant, NewbornInterferon-Induced Helicase, IFIH1Kaplan-Meier EstimateMaleCaspase 3Caspase 9DEAD Box Protein 58DEAD-box RNA HelicasesIFIH1 protein, humanInterferon-Induced Helicase, IFIH1Poly I-CReactive Oxygen SpeciesReceptors, ImmunologicRIGI protein, humanTLR3 protein, humanToll-Like Receptor 3MDA5neuroblastomapoly(I:C)RIG-ITLR3

Identifiers

PMID26208481
PMCPMC4694805

What OpenQuestion holds

Textmetadata
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.