Evidence map›Paper›PMID 24830721›Full record

ArticleCancer research2014

Autophagy inhibition by sustained overproduction of IL6 contributes to arsenic carcinogenesis.

Yuanlin Qi, Mingfang Zhang, Hui Li, Jacqueline A Frank, Lu Dai, Huijuan Liu, Zhuo Zhang, Chi Wang, Gang Chen

Abstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

46 citing papers in PubMed, 78 citations in OpenAlex.

  1. Article
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  9. Review
  10. Review
  11. Article
  12. Review
  13. Paradoxical effects of arsenic in the lungs.Environmental health and preventive medicine · 2021
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Arsenic Exposure and Compromised Protein Quality Control.Chemical research in toxicology · 2020
    Review
  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

9 authors at 3 institutions in 2 countries.

Yuanlin QiAuthors' Affiliations: Department of Molecular & Biomedical Pharmacology, Biochemistry and Molecular Biology and.
Mingfang ZhangAuthors' Affiliations: Department of Molecular & Biomedical Pharmacology, Physiology and Pathophysiology, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian, China.
Hui LiAuthors' Affiliations: Department of Molecular & Biomedical Pharmacology.
Jacqueline A FrankAuthors' Affiliations: Department of Molecular & Biomedical Pharmacology.
Lu DaiGraduate Center for Toxicology, University of Kentucky College of Medicine;
Huijuan LiuAuthors' Affiliations: Department of Molecular & Biomedical Pharmacology.
Zhuo ZhangGraduate Center for Toxicology, University of Kentucky College of Medicine;
Chi WangBiostatistics Shared Resource Facility, Markey Cancer Center and Department of Biostatistics, University of Kentucky College of Public Health, Lexington, Kentucky; and Departments of.
Gang ChenAuthors' Affiliations: Department of Molecular & Biomedical Pharmacology, gangchen6@uky.edu.
University of Kentucky · USFujian Medical University · CNMarkey Cancer Center · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
RAX, PKR and ethanol neurotoxicityR01AA020051 · NIAAA · UNIVERSITY OF KENTUCKY · PI CHEN, GANG · 2012 to 2016
$1.3M
NCI NIH HHS P30 CA177558NIAAA NIH HHS R01 AA020051
6 · The paper itself

Abstract

Chronic inflammation has been implicated as an etiologic factor in cancer, whereas autophagy may help preserve cancer cell survival but exert anti-inflammatory effects. How these phenomenas interact during carcinogenesis remains unclear. We explored this question in a human bronchial epithelial cell-based model of lung carcinogenesis that is mediated by subchronic exposure to arsenic. We found that sustained overexpression of the pro-inflammatory IL6 promoted arsenic-induced cell transformation by inhibiting autophagy. Conversely, strategies to enhance autophagy counteracted the effect of IL6 in the model. These findings were confirmed and extended in a mouse model of arsenic-induced lung cancer. Mechanistic investigations suggested that mTOR inhibition contributed to the activation of autophagy, whereas IL6 overexpression was sufficient to block autophagy by supporting Beclin-1/Mcl-1 interaction. Overall, our findings argued that chronic inflammatory states driven by IL6 could antagonize autophagic states that may help preserve cancer cell survival and promote malignant progression, suggesting a need to uncouple inflammation and autophagy controls to enable tumor progression.

Indexed as

AnimalsApoptosis Regulatory ProteinsArsenicAutophagyBeclin-1Cell LineCell Transformation, NeoplasticEpithelial CellsGranulocyte-Macrophage Colony-Stimulating FactorHumansInterleukin-6MaleMembrane ProteinsMiceMyeloid Cell Leukemia Sequence 1 ProteinProtein BindingApoptosis Regulatory ProteinsArsenicBeclin-1BECN1 protein, humanGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-6Membrane ProteinsMyeloid Cell Leukemia Sequence 1 ProteinRNA, MessengerSTAT3 Transcription FactorTOR Serine-Threonine Kinases

Identifiers

PMID24830721
PMCPMC4102645
OpenAlexW2047533025

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.