Evidence map›Paper›PMID 23761023›Full record

ArticleJournal of neuro-oncology2013

miR-124 radiosensitizes human glioma cells by targeting CDK4.

Xubin Deng, Lei Ma, Minhua Wu, Gong Zhang, Chuan Jin, Yuping Guo, Ruilei Liu

Abstract read
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In one paragraph

Article in Journal of neuro-oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 6% 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

57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 103 citations in OpenAlex.

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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

7 authors at 5 institutions in 1 country.

Xubin DengCancer Institute of Southern Medical University, Guangzhou, People's Republic of China.
Lei Ma
Minhua Wu
Gong Zhang
Chuan Jin
Yuping Guo
Ruilei Liu
Guangzhou Medical University · CNSun Yat-sen University · CNFourth People's Hospital of Taiyuan · CNGuangdong Medical College · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aberrant expression of cyclin-dependent kinase-4 (CDK4) has previously been observed in human brain glioma. Furthermore, it is observed that up-regulation of CDK4 is associated with therapy resistance and relapse. However, the mechanisms behind these phenomena remain unclear. Here, we demonstrated that elevated CDK4 expression is correlated with poor prognosis in glioma after radiotherapy and that CDK4 knockdown conferred radiosensitivity in glioma cell lines. CDK4 was identified as potential downstream target of miR-124 through bioinformatics analysis and dual-firefly luciferase reporter assay. Furthermore, restoration of miR-124 could confer radiosensitivity. Cell differentiation agent-2 (CDA-2) mimicked the effect of miR-124 restoration and CDK4 knockdown, and sensitized xenografts to radiation in an animal model. Our findings demonstrated for the first time that CDK4 was a downstream target of miR-124 and that CDA-2 could radiosensitize Glioblastoma multiforme cells through the MiR-124-CDK4 axis.

Indexed as

AdultAgedAICDA (Activation-Induced Cytidine Deaminase)AnimalsApoptosisBlotting, WesternBrain NeoplasmsCell DifferentiationCell ProliferationCyclin-Dependent Kinase 4Cytidine DeaminaseFemaleFluorescent Antibody TechniqueGlioblastomaHumansImmunoenzyme TechniquesAICDA (Activation-Induced Cytidine Deaminase)CDK4 protein, humanCyclin-Dependent Kinase 4Cytidine DeaminaseLuciferasesMicroRNAsMIRN124 microRNA, humanRNA, MessengerRNA, Small Interfering

Identifiers

PMID23761023
OpenAlexW1966984662

What OpenQuestion holds

Textmetadata
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.