Evidence map›Paper›PMID 28427145›Full record

ArticleOncotarget2017

Uncoupling genotoxic stress responses from circadian control increases susceptibility to mammary carcinogenesis.

Mingzhu Fang, Pamela A Ohman Strickland, Hwan-Goo Kang, Helmut Zarbl

Open access · diamondAbstract readComparative Study
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Liver-gut axis signaling regulates circadian energy metabolism in shift workers.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  2. Disruption of central and peripheral circadian clocks and circadian controlled estrogen receptor rhythms in night shift nurses in working environments.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
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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

4 authors at 3 institutions in 2 countries.

Mingzhu FangSchool of Public Health, Rutgers, The State University of New Jersey, Piscataway, NJ, USA.
Pamela A Ohman StricklandSchool of Public Health, Rutgers, The State University of New Jersey, Piscataway, NJ, USA.
Hwan-Goo KangVeterinary Drugs & Biologics Division, Animal and Plant Quarantine Agency, Gimcheon-si, Gyeongsangbuk-do, Republic of Korea.
Helmut ZarblSchool of Public Health, Rutgers, The State University of New Jersey, Piscataway, NJ, USA.
Rutgers, The State University of New Jersey · USAnimal and Plant Quarantine Agency · KREnvironmental and Occupational Health Sciences Institute · US

Funding

Translational Research Support CoreP30ES005022 · NIEHS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI ROBERT John LAUMBACH · 1988 to 2026
$47.4M
The FHCRC/UW Toxicogenomics ConsortiumU19ES011387 · NIEHS · UNIVERSITY OF WASHINGTON · PI ZARBL, HELMUT · 2001 to 2006
$7.7M
Altered NAD+-dependent Sirt1 as a biomarker of Circadian disruption by shift workR21ES026802 · NIEHS · RBHS-SCHOOL OF PUBLIC HEALTH · PI FANG, MINGZHU · 2017 to 2018
$437k
NIEHS NIH HHS P30 ES005022NIEHS NIH HHS R21 ES026802NIEHS NIH HHS U19 ES011387
6 · The paper itself

Abstract

We previously demonstrated that chemopreventive methylselenocysteine (MSC) prevents N-Nitroso-N-methylurea (NMU)-induced mammary carcinogenesis in the susceptible Fischer 344 (F344) rats by enhancing NAD+-dependent SIRT1 activity, restoring circadian expression of Period 2 (Per2) and circadian controlled genes. Here, we show that compared to the genetically resistant Copenhagen (COP) rat strain, mammary glands of the F344 rats have a 4-hour phase delay in circadian expression of Per2. Consequently, F344 rats failed to increase SIRT1 activity and circadian expression of Per2 and DDRR genes after exposure to NMU. Exposure of COP rats to NMU had the opposite effect, enhancing SIRT1 activity, increasing circadian expression of Per2 and DDRR genes. Significantly, SIRT1 activity and circadian expression of Per2 and DDRR genes in NMU-treated F344 rats on a chemopreventive regimen of MSC approximated those in NMU-treated COP rats. These results indicated that COP rats have an increased capacity to maintain NAD+-dependent SIRT1 activity under genotoxic stress. This contention was supported by increased stability of the period and phase of circadian locomotor activity in COP vs F344 rats exposed to changing light conditions. The increased sensitivity and rapid response of COP to changing light were correlated with the enhanced circadian response of this strain to carcinogen. Disturbance of circadian rhythm by jet lag also disrupted circadian expression of Per2 and DDRR genes, and accelerated mammary tumorigenesis in rodent models. These results suggested that uncoupling of DDRR responses from circadian control by environmental stresses and endogenous factors increases susceptibility to mammary carcinogenesis, possibly by inducing a promutagenic state.

Indexed as

DNA RepairAnimalsCell Transformation, NeoplasticCircadian RhythmDisease Models, AnimalFemaleJet Lag SyndromeMammary Glands, AnimalMammary Neoplasms, ExperimentalMethylnitrosoureaPeriod Circadian ProteinsRatsRats, Inbred F344Sirtuin 1MethylnitrosoureaPer2 protein, ratPeriod Circadian ProteinsSirt1 protein, ratSirtuin 1circadian rhythmDNA damage response and repairgenetic susceptibilityPeriod 2SIRT1

Identifiers

PMID28427145
PMCPMC5464825
OpenAlexW2591563151

What OpenQuestion holds

Textmetadata
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.