Evidence map›Paper›PMID 21561856›Full record

ArticleThe Journal of biological chemistry2011

Caffeine promotes ultraviolet B-induced apoptosis in human keratinocytes without complete DNA repair.

Weinong Han, Mei Ming, Yu-Ying He

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Caffeine Protects Keratinocytes fromInternational journal of molecular sciences · 2024
    Article
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  10. Hyperoside and Quercitrin inAntioxidants (Basel, Switzerland) · 2022
    Article
  11. Review
  12. Review
  13. A Decade of Research on Coffee as an Anticarcinogenic Beverage.Oxidative medicine and cellular longevity · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

Weinong HanSection of Dermatology, Department of Medicine, University of Chicago, Chicago, Illinois 60637, USA.
Mei Ming
Yu-Ying He
University of Chicago · US

Funding

Mechanisms of UVA-induced skin cancerR01ES016936 · NIEHS · UNIVERSITY OF CHICAGO · PI HE, YU-YING · 2010 to 2014
$2.2M
NIEHS NIH HHS ES016936NIEHS NIH HHS R01 ES016936
6 · The paper itself

Abstract

In response to ultraviolet B damage, keratinocytes undergo apoptosis to eliminate damaged cells, thereby preventing tumorigenic transformation. Caffeine, the most widely consumed psychoactive substance, produces complex pharmacological actions; it has been shown to be chemopreventive in non-melamona skin cancer in mice through increasing apoptosis. Here we have investigated the molecular and cellular mechanisms in the pro-apoptotic effect of caffeine on UVB-irradiated human HaCaT keratinocytes. Pretreatment with caffeine increased UVB-induced apoptosis in HaCaT cells. Caffeine blocked UVB-induced Chk1 phosphorylation. In addition, similar to the effect of the PI3K inhibitor LY294002, caffeine also inhibited phosphorylation of AKT and up-regulation of COX-2, two critical oncogenic pathways in skin tumorigenesis. However, phosphorylation of EGFR or ERK was unaffected. Inhibiting ATR pathways by siRNA targeting ATR had little effect on UVB-induced apoptosis or AKT activation, indicating that the inhibitory effect of caffeine on apoptosis and the AKT pathway does not require the ATR pathway. Inhibiting AKT by caffeine blocked UVB-induced COX-2 up-regulation. Expression of constitutively active AKT that was not inhibited by caffeine was found to protect cells from caffeine-promoted apoptosis post-UVB irradiation, indicating that AKT is an essential inhibitory target for caffeine to promote apoptosis. Caffeine specifically sensitized cells with unrepaired DNA damage to UVB-induced apoptosis. These findings indicate that in HaCaT keratinocytes, inhibiting the AKT/COX-2 pathways through an ATR-independent pathway is a critical molecular mechanism by which caffeine promotes UVB-induced apoptosis of unrepaired keratinocytes for elimination.

Indexed as

Ultraviolet RaysAnimalsApoptosisCaffeineCentral Nervous System StimulantsCheckpoint Kinase 1ChromonesCyclooxygenase 2DNA RepairEnzyme InhibitorsHeLa CellsHumansKeratinocytesMiceMorpholinesPhosphatidylinositol 3-Kinases2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneCaffeineCentral Nervous System StimulantsCheckpoint Kinase 1CHEK1 protein, humanChek1 protein, mouseChromonesCyclooxygenase 2Enzyme InhibitorsMorpholinesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein KinasesProto-Oncogene Proteins c-aktPTGS2 protein, human

Identifiers

PMID21561856
PMCPMC3123050
OpenAlexW2030430546

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.