Evidence map›Paper›PMID 24648314›Full record

ArticleThe Journal of pathology2014

Lung tumourigenesis in a conditional Cul4A transgenic mouse model.

Yi-Lin Yang, Ming-Szu Hung, Yang Wang, Jian Ni, Jian-Hua Mao, David Hsieh, Alfred Au, Atul Kumar, David Quigley, Li Tai Fang and 4 more

Abstract read
In one paragraph

Article in The Journal of pathology, 2014. 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
1.4field-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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. CUL4The American journal of pathology · 2021
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. The emerging role for Cullin 4 family of E3 ligases in tumorigenesis.Biochimica et biophysica acta. Reviews on cancer · 2019
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. PR-Set7 is Degraded in a Conditional Cul4A Transgenic Mouse Model of Lung Cancer.Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2015
    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

14 authors at 5 institutions in 3 countries.

Yi-Lin YangDepartment of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.
Ming-Szu Hung
Yang Wang
Jian Ni
Jian-Hua Mao
David Hsieh
Alfred Au
Atul Kumar
David Quigley
Li Tai Fang
Che-Chung Yeh
Zhidong Xu
David M Jablons
Liang You
University of California, San Francisco · USUCSF Helen Diller Family Comprehensive Cancer Center · USBeijing Chao-Yang Hospital · CNLawrence Berkeley National Laboratory · USNational Chiayi University · TW

Funding

The Role of Cul4A in Genome Stability and Cancer DevelopmentR01CA140654 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI YOU, LIANG · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA140654NCI NIH HHS R01 CA140654-01A1
6 · The paper itself

Abstract

Cullin4A (Cul4A) is a scaffold protein that assembles cullin-RING ubiquitin ligase (E3) complexes and regulates many cellular events, including cell survival, development, growth and cell cycle control. Our previous study suggested that Cul4A is oncogenic in vitro, but its oncogenic role in vivo has not been studied. Here, we used a Cul4A transgenic mouse model to study the potential oncogenic role of Cul4A in lung tumour development. After Cul4A over-expression was induced in the lungs for 32 weeks, atypical epithelial cells were observed. After 40 weeks, lung tumours were visible and were characterized as grade I or II adenocarcinomas. Immunohistochemistry (IHC) revealed decreased levels of Cul4A-associated proteins p21(CIP1) and tumour suppressor p19(ARF) in the lung tumours, suggesting that Cul4A regulated their expression in these tumours. Increased levels of p27(KIP1) and p16(INK4a) were also detected in these tumours. Moreover, the protein level of DNA replication licensing factor CDT1 was decreased. Genomic instability in the lung tumours was further analysed by the results from pericentrin protein expression and array comparative genomic hybridization analysis. Furthermore, knocking down Cul4A expression in lung cancer H2170 cells increased their sensitivity to the chemotherapy drug cisplatin in vitro, suggesting that Cul4A over-expression is associated with cisplatin resistance in the cancer cells. Our findings indicate that Cul4A is oncogenic in vivo, and this Cul4A mouse model is a tool in understanding the mechanisms of Cul4A in human cancers and for testing experimental therapies targeting Cul4A.

Indexed as

AdenocarcinomaAdenocarcinoma of LungAnimalsAntineoplastic AgentsCell Cycle ProteinsCell Line, TumorCell SurvivalCell Transformation, NeoplasticCisplatinCullin ProteinsCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p19Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Disease Models, AnimalDNA-Binding ProteinsAntineoplastic AgentsCdkn1a protein, mouseCdkn1b protein, mouseCdkn2d protein, mouseCell Cycle ProteinsCisplatinCUL4A protein, humanCul4a protein, mouseCullin ProteinsCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p19Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27DNA-Binding ProteinsProliferating Cell Nuclear AntigenRis2 protein, mouseAd-Crecell cycleCul4Anon-small cell lung cancertransgenic mouse models

Identifiers

PMID24648314
PMCPMC4084828
OpenAlexW2108240404

What OpenQuestion holds

Textmetadata
LicenceTDM
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.