Evidence map›Paper›PMID 23740091›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2013

Promoter hypermethylation contributes to the frequent suppression of the CDK10 gene in human nasopharyngeal carcinomas.

Yanjie You, Wenjun Yang, Zhizhong Wang, Huimin Zhu, Haijun Li, Canfeng Lin, Yonggang Ran

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  6. Review
  7. Development of a CDK10/CycMFrontiers in chemistry · 2020
    Article
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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.

Yanjie YouDepartment of pharmacy, Luohe Medical College, 148 Daxue-Road, Luohe 462002, China. youyanjie@163.com
Wenjun Yang
Zhizhong Wang
Huimin Zhu
Haijun Li
Canfeng Lin
Yonggang Ran
Luohe Medical College · CNNingxia Medical University · CNAcademy of Military Medical Sciences · CNNeijiang Normal University · CNShantou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrevious studies have shown a down-regulation of the gene encoding cyclin-dependent kinase 10 (CDK10) in hepatocellular carcinomas. Here we provide evidence that down-regulation of the CDK10 gene is mediated by promoter hypermethylation in primary human nasopharyngeal carcinomas (NPC) and NPC-derived cell lines.

methodsRT-PCR, Western blotting, methylation-specific PCR and bisulfite sequencing were performed to assess the expression and methylation status of the CDK10 gene in primary NPC samples, NPC-derived cell lines and patient-derived peripheral blood samples. The NPC-derived cell line CNE-2 was selected for treatment with a methylation inhibitor to restore CDK10 expression. In addition, cell proliferation, invasion and colony formation assays were performed to assess the inhibitory effects of ectopic CDK10 expression in CNE-2 cells.

resultsDown-regulation of CDK10 expression in primary NPC samples (23/40, 57.5%) was found to be significantly correlated with the methylation status of its promoter CpG island (21/40, 52.5%). Demethylation by 5-aza-dC treatment led to reactivation of the CDK10 gene in the CNE-2 cell line. Additionally, exogenous expression of CDK10 in CNE-2 cells strongly suppressed its growth, invasion and colony formation capacities. The high sensitivity (15/40, 37.5%) and specificity (0% false positives) of detecting CDK10 promoter hypermethylation in NPC patient-derived peripheral blood samples suggest that it could be employed as an epigenetic marker for noninvasive cancer diagnosis and recurrence screening.

conclusionOur findings implicate that aberrant methylation of the CDK10 gene promoter occurs frequently in NPC, and that reactivation of CDK10 might be utilized as a novel epigenetic strategy for the treatment of NPC patients.

Indexed as

DNA MethylationAzacitidineBlotting, WesternCell Line, TumorCell ProliferationCell SurvivalCpG IslandsCyclin-Dependent KinasesDecitabineDown-RegulationG1 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticHumansNasopharyngeal NeoplasmsPromoter Regions, GeneticReverse Transcriptase Polymerase Chain ReactionAzacitidineCDK10 protein, humanCyclin-Dependent KinasesDecitabine

Identifiers

PMID23740091
PMCPMC13012668
OpenAlexW2001076827

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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.