Evidence map›Paper›PMID 33155773›Full record

ArticleMolecular genetics & genomic medicine2020

Loss of CDKN2A at chromosome 9 has a poor clinical prognosis and promotes lung cancer progression.

Wei Liu, Congwen Zhuang, Tengfei Huang, Shengsheng Yang, Meiqing Zhang, Baoquan Lin, Yi Jiang

Open access · goldAbstract read
In one paragraph

Article in Molecular genetics & genomic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 16% 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, 28 citations in OpenAlex.

  1. Article
  2. Translational cancer research · 2025
    Article
  3. Article
  4. Clinical significance and prospective mechanism of increased CDKN2A expression in small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Article
  5. Article
  6. Combination Therapy With MDM2 and MEK Inhibitors Is Effective in Patient-Derived Models of Lung Adenocarcinoma With Concurrent Oncogenic Drivers and MDM2 Amplification.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2023
    Article
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  14. Long-Term Clinical Benefit inFrontiers in oncology · 2022
    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 2 institutions in 1 country.

Wei LiuDepartment of Respiratory and Critical Care Medicine, The 900th Hospital of Joint Logistic Support Force, Fuzhou, Fujian, China.
Congwen ZhuangDepartment of Respiratory and Critical Care Medicine, The 900th Hospital of Joint Logistic Support Force, Fuzhou, Fujian, China.
Tengfei HuangDepartment of Respiratory and Critical Care Medicine, The 900th Hospital of Joint Logistic Support Force, Fuzhou, Fujian, China.
Shengsheng YangDepartment of Respiratory and Critical Care Medicine, The 900th Hospital of Joint Logistic Support Force, Fuzhou, Fujian, China.
Meiqing ZhangDepartment of Respiratory and Critical Care Medicine, The 900th Hospital of Joint Logistic Support Force, Fuzhou, Fujian, China.
Baoquan LinDepartment of Thoracic Surgery, The 900th Hospital of Joint Logistic Support Force, Fuzhou, Fujian, China.ORCID 0000-0002-1780-2451
Yi JiangDepartment of Hepatobiliary Surgery, The 900th Hospital of Joint Logistic Support Force, Fuzhou, Fujian, China.
Fuzhou Second Hospital · CNThe 180th Hospital of PLA · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study aimed to identify critical genes involved in the tumor biology of lung cancer via datamining of The Cancer Genome Atlas (TCGA) with special focus on gene copy number variation.

methodsGenomic deletion and amplification were analyzed with cBioportal online tools. Relative expression of Cyclin Dependent Kinase Inhibitor 2A (CDKN2A) was analyzed by both real-time polymerase chain reaction (PCR) and Western blot. The abundance of methylthioadenosine phosphorylase (MTAP) and epithelial-mesenchymal transition markers were analyzed by real-time PCR. Cell proliferation was determined by cell counting kit-8 method and cell viability was measured with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The cell migration and invasion were measured with transwell chamber assay, and migrative capacity was further evaluated by wound healing assay.

resultsWe found the frequent loss of CDKN2A was associated with its downregulation in lung cancer, and siRNA-mediated CDNKN2A knockdown significantly stimulated cell proliferation, invasion, and migration. Mechanistically, we unraveled that MTAP, which was positively correlated with CDKN2A, predominantly mediated the antitumoral function of CDKN2A in lung cancer.

conclusionOur study consolidated the involvement of CDKN2A-MTAP signaling in the context of lung cancer.

Indexed as

A549 CellsBiomarkers, TumorCell MovementCell ProliferationChromosomes, Human, Pair 9Cyclin-Dependent Kinase Inhibitor p16Epithelial-Mesenchymal TransitionHumansLung NeoplasmsPurine-Nucleoside Phosphorylase5'-methylthioadenosine phosphorylaseBiomarkers, TumorCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16Purine-Nucleoside PhosphorylaseCDKN2Acopy number variationlung cancerMTAP

Identifiers

PMID33155773
PMCPMC7767555
OpenAlexW3096874363

What OpenQuestion holds

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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.