Evidence map›Paper›PMID 15067018›Full record

ArticleThe Journal of cell biology2004

PI-3K and Akt are mediators of AP-1 induction by 5-MCDE in mouse epidermal Cl41 cells.

Jingxia Li, Haobin Chen, Moon-Shong Tang, Xianglin Shi, Shantu Amin, Dhimant Desai, Max Costa, Chuanshu Huang

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

25 citing papers in PubMed, 50 citations in OpenAlex.

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  19. Interleukin-32 expression in the pancreas.The Journal of biological chemistry · 2009
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Jingxia LiNelson Institute of Environmental Medicine, New York University School of Medicine, 57 Old Forge Rd., Tuxedo, NY 10987, USA.
Haobin Chen
Moon-Shong Tang
Xianglin Shi
Shantu Amin
Dhimant Desai
Max Costa
Chuanshu Huang
New York University · USInstitute for Cancer Prevention · USChinese Academy of Sciences · CN

Funding

Prevention of Esophageal Cancer with BerriesR01CA103180 · NCI · OHIO STATE UNIVERSITY · PI STONER, GARY · 2003 to 2013
$4.0M
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 CA103180NCI NIH HHS CA112557NCI NIH HHS R01 CA094964NCI NIH HHS R01 CA103180NCI NIH HHS R01 CA112557NIEHS NIH HHS ES012451NIEHS NIH HHS R01 ES012451
6 · The paper itself

Abstract

5-Methylchrysene has been found to be a complete carcinogen in laboratory animals. However, the tumor promotion effects of (+/-)-anti-5-methylchrysene-1,2-diol-3,4-epoxide (5-MCDE) remain unclear. In the present work, we found that 5-MCDE induced marked activator protein-1 (AP-1) activation in Cl41 cells. 5-MCDE also induced a marked activation of phosphatidylinositol 3-kinase (PI-3K). Inhibition of PI-3K impaired 5-MCDE-induced AP-1 transactivation, suggesting that PI-3K is an upstream kinase involved in AP-1 activation by 5-MCDE. Furthermore, we found that Akt is a PI-3K downstream mediator for 5-MCDE-induced AP-1 transactivation, whereas another PI-3K downstream kinase, p70(S6K), was not involved in AP-1 activation by 5-MCDE. Moreover, inhibition of Akt activation blocked 5-MCDE-induced activation of extracellular signal-regulated protein kinases (ERKs) and c-Jun NH(2)-terminal kinases (JNKs), whereas it did not affect p38K activation. Consistently, overexpression of a dominant-negative mutant of ERK2 or JNK1 blocked the AP-1 activation by 5-MCDE. These results demonstrate that 5-MCDE is able to induce AP-1 activation, and the AP-1 induction is specifically through a PI-3K/Akt-dependent and p70(S6K)-independent pathway.

Indexed as

AnimalsCarcinogens, EnvironmentalCell LineChrysenesEnzyme InhibitorsEpidermisGene Expression RegulationJNK Mitogen-Activated Protein KinasesMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 8Mitogen-Activated Protein KinasesMutationNeoplasmsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase Inhibitors1,2-dihydroxy-epoxy-1,2,3,4-tetrahydro-5-methylchryseneCarcinogens, EnvironmentalChrysenesEnzyme InhibitorsJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 8Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRibosomal Protein S6 Kinases, 70-kDaTranscription Factor AP-1

Identifiers

PMID15067018
PMCPMC2172097
OpenAlexW2164983335

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.