Evidence map›Paper›PMID 25925725›Full record

ArticleMedical science monitor basic research2015

The Role of p21 in Apoptosis, Proliferation, Cell Cycle Arrest, and Antioxidant Activity in UVB-Irradiated Human HaCaT Keratinocytes.

Aijun Chen, Xin Huang, Zhenan Xue, Di Cao, Kun Huang, Jin Chen, Yun Pan, Yongliang Gao

Open access · greenAbstract read
In one paragraph

Article in Medical science monitor basic research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.3field-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

39 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Computational Analysis andCurrent medicinal chemistry · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Circadian regulator BMAL1::CLOCK promotes cell proliferation in hepatocellular carcinoma by controlling apoptosis and cell cycle.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Potential Use of Amla (Antioxidants (Basel, Switzerland) · 2021
    Article
  12. Article
  13. Deficiency of miR-208a Exacerbates CClHepatology communications · 2020
    Article
  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

8 authors at 2 institutions in 1 country.

Aijun ChenDepartment of Dermatology, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China (mainland).
Xin HuangDepartment of Traditional Chinese Medicine, Chongqing Medical University, Chongqing, China (mainland).
Zhenan XueDepartment of Dermatology, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China (mainland).
Di CaoDepartment of Dermatology, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China (mainland).
Kun HuangDepartment of Dermatology, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China (mainland).
Jin ChenDepartment of Dermatology, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China (mainland).
Yun PanDepartment of Dermatology, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China (mainland).
Yongliang GaoDepartment of Dermatology, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China (mainland).
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSkin cancer is the most common cancer in the United States, and ultraviolet B (UVB) radiation-induced DNA damage is the major environmental factor underlying skin cancer development. p21, a p53-inducible protein, plays a key role in the cellular response to UVB-induced DNA damage. MATERIAL AND

methodsThrough p21 silencing and overexpression, we investigated the role of p21 in apoptosis, proliferation, cell cycle arrest, and oxidative stress in UVB-irradiated HaCaT keratinocytes.

resultsWe found that UVB exposure induced significant p21 downregulation (p<0.05) and was associated with significantly increased apoptosis, significantly decreased proliferation, and significantly increased G2 phase arrest (p<0.05) in UVB-irradiated HaCaT keratinocytes. p21 silencing significantly promoted apoptosis, significantly inhibited G2 phase arrest, and significantly inhibited proliferation (p<0.05), but after UVB irradiation, p21 silencing demonstrated a less significant pro-apoptotic effect and a more significant inhibition of G2 phase arrest (p<0.05), which was reflected in significantly higher proliferative activity (p<0.05). p21 overexpression acted in an anti-apoptotic manner in the absence of UVB-induced DNA damage but acted in a pro-apoptotic manner in the presence of UVB-induced DNA damage, displaying an "antagonistic duality" similar to other growth-promoting oncoproteins. p53 expression mirrored p21 expression, suggesting a regulatory feedback mechanism between p21 and p53 expression. p21 overexpression significantly downregulated glutathione peroxidase and superoxide dismutase antioxidant activity (p<0.05) while significantly upregulating hydrogen peroxide and malondialdehyde content (p<0.05), suggesting a role in decreasing antioxidant defense capabilities in UVB-irradiated HaCaT keratinocytes.

conclusionsThese findings reveal that p21 may play a key role in HaCaT keratinocytes' response to UVB exposure.

Indexed as

DNA DamageUltraviolet RaysAnalysis of VarianceApoptosisBlotting, WesternCell ProliferationCyclin-Dependent Kinase Inhibitor p21DNA PrimersFlow CytometryG2 Phase Cell Cycle CheckpointsGene Expression RegulationGlutathione PeroxidaseHumansHydrogen PeroxideKeratinocytesMalondialdehydeCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DNA PrimersGlutathione PeroxidaseHydrogen PeroxideMalondialdehydeSuperoxide DismutaseTumor Suppressor Protein p53

Identifiers

PMID25925725
PMCPMC4427023
OpenAlexW2012669917

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.