Evidence map›Paper›PMID 34504274›Full record

ArticleScientific reports2021

Pharmacological inhibition of cryptochrome and REV-ERB promotes DNA repair and cell cycle arrest in cisplatin-treated human cells.

Nadeen Anabtawi, William Cvammen, Michael G Kemp

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.9field-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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Circadian clock and cancer.Military Medical Research · 2026
    Review
  4. The Circadian Modulators as Molecular Targets in Cancer-A Review.International journal of molecular sciences · 2025
    Review
  5. Article
  6. The Influence of Circadian Rhythms on DNA Damage Repair in Skin Photoaging.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Circadian effects on UV-induced damage and mutations.Mutation research. Reviews in mutation research
    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

3 authors at 1 institution in 1 country.

Nadeen AnabtawiDepartment of Pharmacology and Toxicology, Wright State University Boonshoft School of Medicine, Dayton, OH, 45435, USA.
William CvammenDepartment of Pharmacology and Toxicology, Wright State University Boonshoft School of Medicine, Dayton, OH, 45435, USA.
Michael G KempDepartment of Pharmacology and Toxicology, Wright State University Boonshoft School of Medicine, Dayton, OH, 45435, USA. mike.kemp@wright.edu.
Wright State University · US

Funding

DNA damage response kinase signaling in non-replicating human cells and tissuesR01GM130583 · NIGMS · WRIGHT STATE UNIVERSITY · PI KEMP, MICHAEL GEORGE · 2019 to 2023
$1.5M
Mapping DNA Repair and Error-Prone DNA Synthesis in Geriatric SkinI01CX002241 · VA · DAYTON VA MEDICAL CENTER · PI Michael George Kemp · 2021 to 2026
–
NIGMS NIH HHS R01 GM130583
6 · The paper itself

Abstract

Nucleotide excision repair (NER) and cell cycle checkpoints impact the ability of the anti-cancer drug cisplatin to inhibit cell proliferation and induce cell death. Genetic studies have shown that both NER and cell cycle progression are impacted by the circadian clock, which has emerged as a novel pharmacological target for the treatment of various disease states. In this study, cultured human cell lines were treated with combinations of cisplatin and the circadian clock modulating compounds KS15 and SR8278, which enhance circadian clock transcriptional output by inhibiting the activities of the cryptochrome and REV-ERB proteins, respectively. Treatment of cells with KS15 and SR8278 protected cells against the anti-proliferative effects of cisplatin and increased the expression of NER factor XPA and cell cycle regulators Wee1 and p21 at the mRNA and protein level. Correlated with these molecular changes, KS15 and SR8278 treatment resulted in fewer unrepaired cisplatin-DNA adducts in genomic DNA and a higher fraction of cells in the G1 phase of the cell cycle. Thus, the use of pharmacological agents targeting the circadian clock could be a novel approach to modulate the responses of normal and cancer cells to cisplatin chemotherapy regimens.

Indexed as

A549 CellsAntineoplastic AgentsCell Cycle ProteinsCell ProliferationCell SurvivalCircadian ClocksCisplatinCryptochromesDNA AdductsDNA RepairDrug Resistance, NeoplasmG1 Phase Cell Cycle CheckpointsHaCaT CellsHumansIsoquinolinesNuclear Receptor Subfamily 1, Group D, Member 1Antineoplastic AgentsCell Cycle ProteinsCisplatincisplatin-DNA adductCryptochromesDNA AdductsIsoquinolinesNR1D1 protein, humanNuclear Receptor Subfamily 1, Group D, Member 1Protein-Tyrosine KinasesSR 8278ThiophenesWEE1 protein, humanXeroderma Pigmentosum Group A ProteinXPA protein, human

Identifiers

PMID34504274
PMCPMC8429417
OpenAlexW3196762604

What OpenQuestion holds

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LicenceCC BY
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.