Evidence map›Paper›PMID 22696236›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2012

JNK-dependent Stat3 phosphorylation contributes to Akt activation in response to arsenic exposure.

Jia Liu, Bailing Chen, Yongju Lu, Youfei Guan, Fei Chen

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 62 citations in OpenAlex.

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  11. Review
  12. Chronic and acute arsenic exposure enhance EGFR expression via distinct molecular mechanisms.Toxicology in vitro : an international journal published in association with BIBRA · 2020
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Tendon stem/progenitor cells regulate inflammation in tendon healingFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  20. Review
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

5 authors at 3 institutions in 2 countries.

Jia LiuDepartment of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, Michigan 48201, USA.
Bailing Chen
Yongju Lu
Youfei Guan
Fei Chen
Eugene Applebaum College of Pharmacy and Health Sciences · USWayne State University · USPeking University · CN

Funding

Mdig gene and histone demethylation in lung cancerR01ES017217 · NIEHS · WAYNE STATE UNIVERSITY · PI CHEN, FEI · 2009 to 2013
$1.5M
NIEHS NIH HHS R01 ES-017217
6 · The paper itself

Abstract

Environmental exposure to arsenic, especially the trivalent inorganic form (As(3+)), has been linked to human cancers in addition to a number of other diseases including skin lesions, cardiovascular disorders, neuropathy, and internal organ injury. In the present study, we describe a novel signaling axis of the c-Jun NH2 kinase (JNK) and signal transducer and activator of transcription 3 (Stat3) and its involvement in As(3+)-induced Akt activation in human bronchial epithelial cells. As(3+) activates JNK and induces phosphorylation of the Stat3 at serine 727 (S727) in a dose- and time-dependent manner, which occurred concomitantly with Akt activation. Disruption of the JNK signaling pathway by treatment with the JNK inhibitor SP600125, siRNA knockdown of JNK, or genetic deficiency of the JNK1 or JNK2 gene abrogated As(3+)-induced S727 phosphorylation of Stat3, Akt activation, and the consequent release of vascular endothelial growth factor (VEGF) and migration of the cells. Similarly, pretreatment of the cells with Stat3 inhibitor or Stat3 siRNA prevented Akt activation and VEGF release from the cells in response to As(3+) treatment. Taken together, these data revealed a new signaling mechanism that might be pivotal in As(3+)-induced malignant transformation of the cells by linking the key stress signaling pathway, JNK, to the activation of Stat3 and the carcinogenic kinase, Akt.

Indexed as

ArsenicCell LineCoculture TechniquesEnzyme ActivationEnzyme-Linked Immunosorbent AssayHumansInterleukin-6MAP Kinase Kinase 4PhosphorylationProto-Oncogene Proteins c-aktSerineSTAT3 Transcription FactorVascular Endothelial Growth Factor AArsenicInterleukin-6MAP Kinase Kinase 4Proto-Oncogene Proteins c-aktSerineSTAT3 protein, humanSTAT3 Transcription FactorVascular Endothelial Growth Factor A

Identifiers

PMID22696236
PMCPMC3529643
OpenAlexW2169363183

What Socratic holds

Textmetadata
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 Socratic graph.