Evidence map›Paper›PMID 25413624›Full record

ArticleMolecular cancer2014

CUL4A overexpression enhances lung tumor growth and sensitizes lung cancer cells to erlotinib via transcriptional regulation of EGFR.

Yunshan Wang, Pengju Zhang, Ziming Liu, Qin Wang, Mingxin Wen, Yuli Wang, Hongtu Yuan, Jian-Hua Mao, Guangwei Wei

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 57 citations in OpenAlex.

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  7. Progesterone activates GPR126 to promote breast cancer development via the Gi pathway.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. CUL4The American journal of pathology · 2021
    Article
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  19. The emerging role for Cullin 4 family of E3 ligases in tumorigenesis.Biochimica et biophysica acta. Reviews on cancer · 2019
    Review
  20. 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

9 authors at 5 institutions in 2 countries.

Yunshan Wang
Pengju Zhang
Ziming Liu
Qin Wang
Mingxin Wen
Yuli Wang
Hongtu Yuan
Jian-Hua Mao
Guangwei WeiDepartment of Anatomy and Key Laboratory of Experimental Teratology, Ministry of Education, Shandong University School of Medicine, 44 Wenhua Xi Road, Jinan, Shandong 250012, P,R, China. gwwei@yahoo.com.
Shandong University · CNFourth People’s Hospital of Jinan · CNLawrence Berkeley National Laboratory · USQilu Hospital of Shandong University · CNShandong Tumor Hospital · CN

Funding

The Role of Fbxw7 in genetic instability and cancerR01CA116481 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MAO, JIAN-HUA · 2008 to 2012
$1.7M
NCI NIH HHS R01 CA116481
6 · The paper itself

Abstract

backgroundCUL4A has been proposed as oncogene in several types of human cancer, but its clinical significance and functional role in human non-small cell lung cancer (NSCLC) remain unclear.

methodsExpression level of CUL4A was examined by RT-PCR and Western blot. Forced expression of CUL4A was mediated by retroviruses, and CUL4A silencing by shRNAs expressing lentiviruses. Growth capacity of lung cancer cells was measured by MTT in vitro and tumorigenesis in vivo, respectively.

resultsWe found that CUL4A was highly expressed in human lung cancer tissues and lung cancer cell lines, and this elevated expression positively correlated with disease progression and prognosis. Overexpression of CUL4A in human lung cancer cell lines increased cell proliferation, inhibited apoptosis, and subsequently conferred resistance to chemotherapy. On other hand, silencing CUL4A expression in NSCLC cells reduced proliferation, promoted apoptosis and resulted in tumor growth inhibition in cancer xenograft model. Mechanistically, we revealed CUL4A regulated EGFR transcriptional expression and activation, and subsequently activated AKT. Targeted inhibition of EGFR activity blocked these CUL4A induced oncogenic activities.

conclusionsOur results highlight the significance of CUL4A in NSCLC and suggest that CUL4A could be a promising therapy target and a potential biomarker for prognosis and EGFR target therapy in NSCLC patients.

Indexed as

ApoptosisCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCullin ProteinsErbB ReceptorsErlotinib HydrochlorideFemaleHumansLung NeoplasmsMaleMiddle AgedProtein Kinase InhibitorsQuinazolinesTranscription, GeneticCUL4A protein, humanCullin ProteinsEGFR protein, humanErbB ReceptorsErlotinib HydrochlorideProtein Kinase InhibitorsQuinazolines

Identifiers

PMID25413624
PMCPMC4246448
OpenAlexW2096586295

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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.