Evidence map›Paper›PMID 25319395›Full record

ArticleMolecular cancer therapeutics2014

Involvement of microRNA-24 and DNA methylation in resistance of nasopharyngeal carcinoma to ionizing radiation.

Sumei Wang, Rong Zhang, Francois X Claret, Huiling Yang

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

42 citing papers in PubMed, 60 citations in OpenAlex.

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  6. DNA repair in tumor radioresistance: insights from fruit flies genetics.Cellular oncology (Dordrecht, Netherlands) · 2024
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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

4 authors at 2 institutions in 2 countries.

Sumei WangDepartment of Pathophysiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, Guangdong, P.R. China. Department of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Rong ZhangDepartment of Pathophysiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, Guangdong, P.R. China. State Key Laboratory of Oncology in South China, Sun Yat-Sen University, Guangzhou, Guangdong, P.R. China.
Francois X ClaretDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas. Experimental Therapeutics Academic Program and Cancer Biology Program, The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, Texas. fxclaret@mdanderson.org hlyangsums@hotmail.com.
Huiling YangDepartment of Pathophysiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, Guangdong, P.R. China. fxclaret@mdanderson.org hlyangsums@hotmail.com.
Sun Yat-sen University · CNThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Targeting JAB1 Oncogenic Function in Breast CancerR01CA090853 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI CLARET, FRANCOIS X · 2002 to 2011
$2.5M
NCI NIH HHS CA16672NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA090853NCI NIH HHS R01-CA90853
6 · The paper itself

Abstract

Nasopharyngeal carcinoma (NPC) is a malignant tumor originating in the epithelium. Radiotherapy is the standard therapy, but tumor resistance to this treatment reduces the 5-year patient survival rate dramatically. Studies are urgently needed to elucidate the mechanism of NPC radioresistance. Epigenetics--particularly microRNAs (miRNA) and DNA methylation--plays an important role in carcinogenesis and oncotherapy. We used qRT-PCR analysis and identified an miRNA signature from differentially expressed miRNAs. Our objectives were to identify the role of miR24 in NPC tumorigenesis and radioresistance and to identify the mechanisms by which miR24 is regulated. We found that miR24 inhibited NPC cell growth, promoted cell apoptosis, and suppressed the growth of NPC xenografts. We showed that miR24 was significantly downregulated in recurrent NPC tissues. When combined with irradiation, miR24 acted as a radiosensitizer in NPC cells. One of the miR24 precursors was embedded in a CpG island. Aberrant DNA methylation was involved in NPC response to radiotherapy, which linked inactivation of miR24 through hypermethylation of its precursor promoter with NPC radioresistance. Treating NPC cells with the DNA-hypomethylating agent 5-aza-2'-deoxycytidine compensated for the reduced miR24 expression. Together, our findings showed that miR24 was negatively regulated by hypermethylation of its precursor promoter in NPC radioresistance. Our findings defined a central role for miR24 as a tumor-suppressive miRNA in NPC and suggested its use in novel strategies for treatment of this cancer.

Indexed as

DNA MethylationRadiation, IonizingAnimalsAzacitidineCarcinomaCell Line, TumorCell ProliferationCluster AnalysisDecitabineDisease Models, AnimalGene Expression ProfilingGene Expression Regulation, NeoplasticHistonesHumansMaleMiceAzacitidineDecitabineHistonesMicroRNAsMIRN24 microRNA, human

Identifiers

PMID25319395
PMCPMC4258432
OpenAlexW2136542410

What OpenQuestion holds

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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.