Evidence map›Paper›PMID 23212914›Full record

ArticleThe Journal of biological chemistry2013

Autophagy controls p38 activation to promote cell survival under genotoxic stress.

Lei Qiang, Chunli Wu, Mei Ming, Benoit Viollet, Yu-Ying He

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

63 citing papers in PubMed, 108 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Autophagy regulates tumor growth and metastasis.bioRxiv : the preprint server for biology · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Autophagy and Skin Diseases.Frontiers in pharmacology · 2022
    Review
  19. Article
  20. METTL14 facilitates global genome repair and suppresses skin tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article

3 more citing papers are in PubMed but not listed here.

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 3 countries.

Lei QiangSection of Dermatology, Department of Medicine, University of Chicago, Chicago, Illinois 60637, USA.
Chunli Wu
Mei Ming
Benoit Viollet
Yu-Ying He
University of Chicago · USChina Medical University · CNInstitut Cochin · FR

Funding

VIRAL ONCOLOGY CORE FACILITYP30CA014599 · NCI · UNIVERSITY OF CHICAGO · PI THOMAS F GAJEWSKI · 1985 to 2026
$122.1M
TRANSLATIONAL RESEARCH UNIVERSITY OF CHICAGO: CLINICAL TRIALSUL1RR024999 · NCRR · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2007 to 2011
$25.3M
Mechanisms of UVA-induced skin cancerR01ES016936 · NIEHS · UNIVERSITY OF CHICAGO · PI HE, YU-YING · 2010 to 2014
$2.2M
NCI NIH HHS P30 CA014599NCRR NIH HHS UL1 RR024999NCRR NIH HHS UL1RR024999NIEHS NIH HHS ES016936NIEHS NIH HHS R01 ES016936
6 · The paper itself

Abstract

Deregulated cell survival under carcinogen-induced genotoxic stress is vital for cancer development. One of the cellular processes critical for cell survival under metabolic stress and energy starvation is autophagy, a catabolic process involved in capture and delivery of cytoplasmic components to lysosomes for degradation. However, the role of autophagy following carcinogen-induced genotoxic stress remains unclear. Here we show that UVB radiation, a known human skin carcinogen that operates by causing DNA damage, induced autophagy and autophagic flux through AMP kinase activation. Autophagy deficiency sensitizes cells to UVB-induced apoptosis through increasing p62-dependent activation of the stress-activated protein kinase p38. Compared with normal human skin, autophagy was activated in human squamous cell carcinomas, in association with decreased phosphorylation of p38, and increased phosphorylation of ATR and formation of γ-H2AX, two markers of DNA damage response. Our results demonstrate that autophagy promotes cell survival through suppressing p62-mediated p38 activation and thus may facilitate tumor development under genotoxic stress. These findings suggest that autophagy plays an oncogenic role in epithelial carcinogenesis by promoting cell survival.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsAutophagyCarcinoma, Squamous CellCell Cycle ProteinsCells, CulturedCell SurvivalCell Transformation, NeoplasticDNA DamageEnzyme ActivationEpidermal CellsEpidermisFibroblastsGene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingAtaxia Telangiectasia Mutated ProteinsATR protein, humanCell Cycle ProteinsH2AX protein, humanHistonesp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesSequestosome-1 ProteinSQSTM1 protein, human

Identifiers

PMID23212914
PMCPMC3548470
OpenAlexW2153377288

What OpenQuestion 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 OpenQuestion graph.