Evidence map›Paper›PMID 19519318›Full record

ArticleCurrent cancer drug targets2009

PI3K/Akt/JNK/c-Jun signaling pathway is a mediator for arsenite-induced cyclin D1 expression and cell growth in human bronchial epithelial cells.

Jin Ding, Beifang Ning, Yi Huang, Dongyun Zhang, Jingxia Li, Chang-Yan Chen, Chuanshu Huang

Abstract read
In one paragraph

Article in Current cancer drug targets, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-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

13 citing papers in PubMed, 32 citations in OpenAlex.

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  12. Histone deacetylase 6 associates with ribosomes and regulates de novo protein translation during arsenite stress.Toxicological sciences : an official journal of the Society of Toxicology · 2012
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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 1 institution in 1 country.

Jin DingNelson Institute of Environmental Medicine, New York University School of Medicine, 57 Old Forge Road, Tuxedo, NY 10987, USA. dingjin@yahoo.cn
Beifang Ning
Yi Huang
Dongyun Zhang
Jingxia Li
Chang-Yan Chen
Chuanshu Huang
New York University · US

Funding

RESEARCH IN ENVIRONMENTAL HEALTH SCIENCES (CENTER GRANT)P30ES000260 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX · 1985 to 2020
$26.1M
Water/sediment &model &criteria for arsenic &chromeP42ES010344 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI COSTA, MAX · 2000 to 2010
$15.0M
Molecular Mechanisms of Nickel-Induced TumorigenicityR01CA112557 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUANG, CHUANSHU · 2004 to 2016
$2.9M
Mechanisms of Tumor Promotion Effects of B[a]PDER01ES012451 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUANG, CHUANSHU · 2004 to 2008
$1.7M
Effects of Arsenic on PI-3K Signaling PathwayR01CA094964 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUANG, CHUANSHU · 2004 to 2007
$1.1M
NCI NIH HHS CA094964NCI NIH HHS CA112557NCI NIH HHS R01 CA094964NCI NIH HHS R01 CA112557NIEHS NIH HHS ES000260NIEHS NIH HHS ES010344NIEHS NIH HHS ES012451NIEHS NIH HHS P30 ES000260NIEHS NIH HHS P42 ES010344NIEHS NIH HHS R01 ES012451
6 · The paper itself

Abstract

Arsenite exposure is associated with an increased risk of human lung cancer. However, the molecular mechanisms underlying the arsenite-induced human lung carcinogenesis remain elusive. In this study, we demonstrated that arsenite upregulates cyclin D1 expression/activity to promote the growth of human bronchial epithelial Beas-2B cells. In this process, the JNKs (c-Jun N-terminal kinases)/c-Jun cascade is elicited. The inhibition of JNKs or c-Jun by chemical or genetic inhibitors blocks the cyclin D1 induction mediated by arsenite. Furthermore, using a loss of function mutant of p85 (Deltap85, a subunit of PI3K) or dominant-negative Akt (DN-Akt), we showed that PI3K and Akt act as the upstream regulators of JNKs and c-Jun in arsenite-mediated growth promotion. Overall, our data suggest a pathway of PI-3K/Akt/JNK/c-Jun/cylin D1 signaling in response to arsenite in human bronchial epithelial cells.

Indexed as

ArsenitesBronchiCell ProliferationCells, CulturedCyclin D1HumansJNK Mitogen-Activated Protein KinasesNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-junRespiratory MucosaSignal TransductionUp-RegulationarseniteArsenitesCyclin D1JNK Mitogen-Activated Protein KinasesNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-jun

Identifiers

PMID19519318
PMCPMC3758122
OpenAlexW2160552772

What OpenQuestion holds

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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.