Evidence map›Paper›PMID 26945572›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

JMJD1A promotes tumorigenesis and forms a feedback loop with EZH2/let-7c in NSCLC cells.

Min Zhan, Feiqiu Wen, Lijuan Liu, Zebin Chen, Hong Wei, Honghao Zhou

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Targeting Epigenetics in Lung Cancer.Cold Spring Harbor perspectives in medicine · 2021
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Lung Cancer Therapy Targeting Histone Methylation: Opportunities and Challenges.Computational and structural biotechnology journal · 2018
    Review
  14. Article
  15. Article
  16. Article
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 at 3 institutions in 1 country.

Min ZhanShen Zhen Children's Hospital, Shenzhen, 510038, People's Republic of China.
Feiqiu WenShen Zhen Children's Hospital, Shenzhen, 510038, People's Republic of China.
Lijuan LiuJiangxi Provincial Cancer Hospital, Nanchang, 330029, People's Republic of China.
Zebin ChenShen Zhen Children's Hospital, Shenzhen, 510038, People's Republic of China.
Hong WeiShen Zhen Children's Hospital, Shenzhen, 510038, People's Republic of China.
Honghao ZhouDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, People's Republic of China. hhzhou2003@163.com.
Shenzhen Children's Hospital · CNCentral South University · CNJiangxi Provincial Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the most common cause of cancer-related deaths worldwide, and non-small cell lung cancer (NSCLC) accounts for 80 to 85 % of all lung cancer. Although the standard treatment regimen has been established, long-term survival for NSCLC patients is still generally poor. The histone demethylase Jumonji domain containing 1A (JMJD1A) has been proposed as an oncogene in several types of human cancer, but its clinical significance and functional roles in NSCLC remain largely unclear. In the present study, JMJD1A was frequently upregulated in NSCLC compared with para-carcinoma tissues. JMJD1A knockdown significantly inhibited NSCLC cell growth, migration, and invasion in vitro and tumorigenesis in vivo. Further experiments demonstrated that JMJD1A knockdown could decrease the expression of EZH2, which has been shown to play a crucial role in the carcinogenesis of NSCLC and, in turn, increase the expression of anti-tumor microRNA let-7c. Also, let-7c directly targeted the 3'-untranslated regions of JMJD1A and EZH2. Taken together, JMJD1A could promote NSCLC tumorigenesis. JMJD1A/EZH2/let-7c constituted a feedback loop and might represent a promising therapeutic target for NSCLC.

Indexed as

AnimalsBlotting, WesternCarcinogenesisCarcinoma, Non-Small-Cell LungCell Line, TumorCell Transformation, NeoplasticEnhancer of Zeste Homolog 2 ProteinFeedback, PhysiologicalGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeterograftsHumansImmunohistochemistryJumonji Domain-Containing Histone DemethylasesLung NeoplasmsMaleEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanJumonji Domain-Containing Histone DemethylasesKDM3A protein, humanMicroRNAsmirnlet7 microRNA, humanEZH2FeedbackJMJD1ALet-7cNSCLCTumorigenesis

Identifiers

PMID26945572
OpenAlexW2289445514

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.