Evidence map›Paper›PMID 25321470›Full record

ArticleCell death & disease2014

Reprogramming the fate of human glioma cells to impede brain tumor development.

Z Su, T Zang, M-L Liu, L-L Wang, W Niu, C-L Zhang

Abstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
–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

41 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Molecular therapy. Oncology · 2026
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  17. Biomimetic three-dimensional glioma model printedInternational journal of bioprinting · 2023
    Article
  18. Review
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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.

Z Su1] Department of Molecular Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390-9148, USA [2] Institute of Neuroscience and Key Laboratory of Molecular Neurobiology of Ministry of Education, Neuroscience Research Center of Changzheng Hospital, Second Military Medical University, 800 Xiangyin Road, Shanghai 200433, China.
T ZangDepartment of Molecular Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390-9148, USA.
M-L LiuDepartment of Molecular Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390-9148, USA.
L-L WangDepartment of Molecular Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390-9148, USA.
W NiuDepartment of Molecular Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390-9148, USA.
C-L ZhangDepartment of Molecular Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390-9148, USA.

Funding

Reprogramming reactive glial cells into functional new neurons after SCIR01NS111776 · NINDS · INDIANA UNIVERSITY INDIANAPOLIS · PI WU, WEI, ZHANG, CHUN-LI · 2020 to 2024
$2.4M
In Vivo Reprogramming of Glial Fate for Spinal Cord RepairR01NS088095 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI ZHANG, CHUN-LI · 2014 to 2018
$1.7M
Transcriptional Control of Adult Neural Stem CellsR01NS070981 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI ZHANG, CHUN-LI · 2011 to 2015
$1.7M
NINDS NIH HHS R01 NS070981NINDS NIH HHS R01NS070981NINDS NIH HHS R01 NS088095NINDS NIH HHS R01NS088095NINDS NIH HHS R01 NS111776
6 · The paper itself

Abstract

Malignant gliomas, the most common solid tumors in the central nervous system, are essentially incurable due to their rapid growth and very invasive nature. One potential approach to eradicating glioma cells is to force these cells to undergo terminal differentiation and, in the process, to irreversible postmitotic arrest. Here, we show that neurogenin 2 (NGN2, also known as NEUROG2) synergizes with sex-determining region Y-box 11 (SOX11) to very efficiently convert human glioma cells to terminally differentiated neuron-like cells in both cell culture and adult mouse brains. These cells exhibit neuronal morphology, marker expression, and electrophysiological properties. The conversion process is accompanied by cell cycle exit, which dramatically inhibits glioma cell proliferation and tumor development after orthotopic transplantation. Most importantly, intracranial injection of NGN2- and SOX11-expressing virus into the tumor mass also curtails glioma growth and significantly improves survival of tumor-bearing mice. Taken together, this study shows a simple and highly efficient strategy for reprogramming malignant glioma cells into postmitotic cells, which might be a promising therapeutic approach for brain tumors.

Indexed as

Cell LineageCellular ReprogrammingAnimalsBasic Helix-Loop-Helix ProteinsBrain NeoplasmsCarcinogenesisCell CycleCell Line, TumorCell ProliferationGliomaHEK293 CellsHumansMiceNerve Tissue ProteinsNeuronsSOXC Transcription FactorsBasic Helix-Loop-Helix ProteinsNerve Tissue ProteinsNEUROG2 protein, humanSOX11 protein, humanSOXC Transcription Factors

Identifiers

PMID25321470
PMCPMC4649522

What OpenQuestion holds

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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.