Evidence map›Paper›PMID 27472461›Full record

ArticleOncotarget2016

Novel function of MDA-9/Syntenin (SDCBP) as a regulator of survival and stemness in glioma stem cells.

Sarmistha Talukdar, Swadesh K Das, Anjan K Pradhan, Luni Emdad, Xue-Ning Shen, Jolene J Windle, Devanand Sarkar, Paul B Fisher

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Article
  2. Review
  3. MDA-9/Syntenin in the tumor and microenvironment defines prostate cancer bone metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  4. Article
  5. Recognition of a Novel Gene Signature for Human Glioblastoma.International journal of molecular sciences · 2022
    Article
  6. Article
  7. Pharmacological inhibition of MDA-9/Syntenin blocks breast cancer metastasis through suppression of IL-1β.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Syntenin: PDZ Protein Regulating Signaling Pathways and Cellular Functions.International journal of molecular sciences · 2019
    Review
  15. Lung Adenocarcinoma Syndecan-2 Potentiates Cell Invasiveness.American journal of respiratory cell and molecular biology · 2019
    Article
  16. A PDZ Protein MDA-9/Syntenin: As a Target for Cancer Therapy.Computational and structural biotechnology journal · 2019
    Review
  17. Article
  18. MDA-9/Syntenin regulates protective autophagy in anoikis-resistant glioma stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  19. Review
  20. Inhibition of radiation-induced glioblastoma invasion by genetic and pharmacological targeting of MDA-9/Syntenin.Proceedings of the National Academy of Sciences of the United States of America · 2017
    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.

Sarmistha TalukdarDepartment of Human and Molecular Genetics, Virginia Commonwealth University, School of Medicine, Richmond, VA, USA.
Swadesh K DasDepartment of Human and Molecular Genetics, Virginia Commonwealth University, School of Medicine, Richmond, VA, USA.
Anjan K PradhanDepartment of Human and Molecular Genetics, Virginia Commonwealth University, School of Medicine, Richmond, VA, USA.
Luni EmdadDepartment of Human and Molecular Genetics, Virginia Commonwealth University, School of Medicine, Richmond, VA, USA.
Xue-Ning ShenDepartment of Human and Molecular Genetics, Virginia Commonwealth University, School of Medicine, Richmond, VA, USA.
Jolene J WindleDepartment of Human and Molecular Genetics, Virginia Commonwealth University, School of Medicine, Richmond, VA, USA.
Devanand SarkarDepartment of Human and Molecular Genetics, Virginia Commonwealth University, School of Medicine, Richmond, VA, USA.
Paul B FisherDepartment of Human and Molecular Genetics, Virginia Commonwealth University, School of Medicine, Richmond, VA, USA.

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Keri R Maher · 1985 to 2026
$51.0M
VCU Neuroscience Center Core GrantP30NS047463 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI POVLISHOCK, JOHN T · 2003 to 2013
$5.0M
AEG-1: Novel Gene Involved in Malignant GliomaR01CA134721 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI FISHER, PAUL B · 2009 to 2013
$1.5M
NCI NIH HHS P30 CA016059NCI NIH HHS R01 CA134721NINDS NIH HHS P30 NS047463
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is an aggressive cancer with current therapies only marginally impacting on patient survival. Glioma stem cells (GSCs), a subpopulation of highly tumorigenic cells, are considered major contributors to glioma progression and play seminal roles in therapy resistance, immune evasion and increased invasion. Despite clinical relevance, effective/selective therapeutic targeting strategies for GSCs do not exist, potentially due to the lack of a definitive understanding of key regulators of GSCs. Consequently, there is a pressing need to identify therapeutic targets and novel options to effectively target this therapy-resistant cell population. The precise roles of GSCs in governing GBM development, progression and prognosis are under intense scrutiny, but key upstream regulatory genes remain speculative. MDA-9/Syntenin (SDCBP), a scaffold protein, regulates tumor pathogenesis in multiple cancers. Highly aggressive cancers like GBM express elevated levels of MDA-9 and contain increased populations of GSCs. We now uncover a unique function of MDA-9 as a facilitator and determinant of glioma stemness and survival. Mechanistically, MDA-9 regulates multiple stemness genes (Nanog, Oct4 and Sox2) through activation of STAT3. MDA-9 controls survival of GSCs by activating the NOTCH1 pathway through phospho-Src and DLL1. Once activated, cleaved NOTCH1 regulates C-Myc expression through RBPJK, thereby facilitating GSC growth and proliferation. Knockdown of MDA-9 affects the NOTCH1/C-Myc and p-STAT3/Nanog pathways causing a loss of stemness and initiation of apoptosis in GSCs. Our data uncover a previously unidentified relationship between MDA-9 and GSCs, reinforcing relevance of this gene as a potential therapeutic target in GBM.

Indexed as

AnimalsAstrocytesBrain NeoplasmsCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p27FemaleGliomaHumansMiceNeoplastic Stem CellsProto-Oncogene Proteins c-mycReceptor, Notch1STAT3 Transcription FactorSynteninsCDKN1B protein, humanCyclin-Dependent Kinase Inhibitor p27MYC protein, humanProto-Oncogene Proteins c-mycReceptor, Notch1SDCBP protein, humanSTAT3 Transcription FactorSynteninsapoptosisglioma stem cellsMDA-9/Syntenin (SDCBP)stemnesssurvival

Identifiers

PMID27472461
PMCPMC5342330

What OpenQuestion holds

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Registered trials

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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.