Evidence map›Paper›PMID 27396340›Full record

ArticleCell reports2016

Post-translational Modifications of OLIG2 Regulate Glioma Invasion through the TGF-β Pathway.

Shiv K Singh, Roberto Fiorelli, Robert Kupp, Sindhu Rajan, Emily Szeto, Costanza Lo Cascio, Cecile L Maire, Yu Sun, John A Alberta, Jennifer M Eschbacher and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 60 citations in OpenAlex.

  1. Understanding Glioblastoma Dynamics Using 3D Organoids and Engineered Extracellular Matrix.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. OLIG2 Is a Determinant for the Relapse of MYC-Amplified Medulloblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. The Role of Neurodevelopmental Pathways in Brain Tumors.Frontiers in cell and developmental biology · 2021
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 6 institutions in 1 country.

Shiv K SinghDivision of Neurobiology, Barrow Brain Tumor Research Center, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013, USA.
Roberto FiorelliDivision of Neurobiology, Barrow Brain Tumor Research Center, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013, USA.
Robert KuppDivision of Neurobiology, Barrow Brain Tumor Research Center, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013, USA.
Sindhu RajanDivision of Neurobiology, Barrow Brain Tumor Research Center, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013, USA.
Emily SzetoDivision of Neurobiology, Barrow Brain Tumor Research Center, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013, USA.
Costanza Lo CascioDivision of Neurobiology, Barrow Brain Tumor Research Center, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013, USA.
Cecile L MaireDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Yu SunDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
John A AlbertaDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
Jennifer M EschbacherDivision of Neuropathology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013, USA.
Keith L LigonDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Michael E BerensCancer and Cell Biology Division, Translational Genomics Institute, Phoenix, AZ 85004, USA.
Nader SanaiDivision of Neurobiology, Barrow Brain Tumor Research Center, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013, USA.
Shwetal MehtaDivision of Neurobiology, Barrow Brain Tumor Research Center, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013, USA. Electronic address: shwetal.mehta@dignityhealth.org.
Barrow Neurological Institute · USDana-Farber Cancer Institute · USSt. Joseph's Hospital and Medical Center · USBrigham and Women's Hospital · USHarvard University · USTranslational Genomics Research Institute · US

Funding

Molecular Mechanisms Underlying Glioma Invasion of the Human Subventricular ZoneR01NS082745 · NINDS · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI SANAI, NADER · 2013 to 2017
$1.8M
Targeting Olig2 Co-regulators for Malignant Glioma TherapyR01NS088648 · NINDS · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI MEHTA, SHWETAL · 2015 to 2019
$1.7M
Intraoperative confocal microscopy for quantitative delineation of low-grade glioR01CA175391 · NCI · UNIVERSITY OF WASHINGTON · PI LIU, JONATHAN T.C., SANAI, NADER · 2014 to 2018
$1.7M
NCI NIH HHS R01 CA175391NINDS NIH HHS R01 NS082745NINDS NIH HHS R01 NS088648
6 · The paper itself

Abstract

In glioblastoma, invasion and proliferation are presumed to be mutually exclusive events; however, the molecular mechanisms that mediate this switch at the cellular level remain elusive. Previously, we have shown that phospho-OLIG2, a central-nervous-system-specific transcription factor, is essential for tumor growth and proliferation. Here, we show that the modulation of OLIG2 phosphorylation can trigger a switch between proliferation and invasion. Glioma cells with unphosphorylated OLIG2(S10, S13, S14) are highly migratory and invasive, both in vitro and in vivo. Mechanistically, unphosphorylated OLIG2 induces TGF-β2 expression and promotes invasive mesenchymal properties in glioma cells. Inhibition of the TGF-β2 pathway blocks this OLIG2-dependent invasion. Furthermore, ectopic expression of phosphomimetic Olig2 is sufficient to block TGF-β2-mediated invasion and reduce expression of invasion genes (ZEB1 and CD44). Our results not only provide a mechanistic insight into how cells switch from proliferation to invasion but also offer therapeutic opportunities for inhibiting dissemination of gliomas.

Indexed as

AnimalsCell Line, TumorCell ProliferationGlioblastomaHumansHyaluronan ReceptorsMiceMice, NudeNeoplasm InvasivenessOligodendrocyte Transcription Factor 2PhosphorylationProtein Processing, Post-TranslationalSignal TransductionTransforming Growth Factor betaZinc Finger E-box-Binding Homeobox 1Hyaluronan ReceptorsOLIG2 protein, humanOligodendrocyte Transcription Factor 2Transforming Growth Factor betaZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID27396340
PMCPMC4963280
OpenAlexW2473795771

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.