Evidence map›Paper›PMID 28196531›Full record

ArticleBMC biology2017

Enhancing circadian clock function in cancer cells inhibits tumor growth.

Silke Kiessling, Lou Beaulieu-Laroche, Ian D Blum, Dominic Landgraf, David K Welsh, Kai-Florian Storch, Nathalie Labrecque, Nicolas Cermakian

Open access · goldAbstract read
In one paragraph

Article in BMC biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
10.9field-weighted citation impact, top 1% 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

106 citing papers in PubMed, 180 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Circadian Behavioral and Bioluminescence Rhythms in theJournal of biological rhythms · 2026
    Article
  5. Review
  6. Article
  7. Review
  8. Circadian genesJournal of Zhejiang University. Science. B · 2025
    Review
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  10. Article
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46 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

8 authors at 3 institutions in 3 countries.

Silke KiesslingDouglas Mental Health University Institute, Montreal, QC, H4H 1R3, Canada.
Lou Beaulieu-LarocheDouglas Mental Health University Institute, Montreal, QC, H4H 1R3, Canada.
Ian D BlumDouglas Mental Health University Institute, Montreal, QC, H4H 1R3, Canada.
Dominic LandgrafCenter for Circadian Biology and Department of Psychiatry, University of California, San Diego, CA, 92037, USA.
David K WelshCenter for Circadian Biology and Department of Psychiatry, University of California, San Diego, CA, 92037, USA.
Kai-Florian StorchDouglas Mental Health University Institute, Montreal, QC, H4H 1R3, Canada.
Nathalie LabrecqueMaisonneuve-Rosemont Hospital Research Centre, Montreal, QC, H1T 2M4, Canada.
Nicolas CermakianDouglas Mental Health University Institute, Montreal, QC, H4H 1R3, Canada. nicolas.cermakian@mcgill.ca.ORCID 0000-0003-4517-9131
Douglas Mental Health University Institute · CAUniversity of California San Diego · USHôpital Maisonneuve-Rosemont · CA

Funding

Cellular Circadian Clocks in Mood DisordersI01BX001146 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI WELSH, DAVID K · 2012 to 2020
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BLRD VA I01 BX001146CIHR MOP-119322
6 · The paper itself

Abstract

backgroundCircadian clocks control cell cycle factors, and circadian disruption promotes cancer. To address whether enhancing circadian rhythmicity in tumor cells affects cell cycle progression and reduces proliferation, we compared growth and cell cycle events of B16 melanoma cells and tumors with either a functional or dysfunctional clock.

resultsWe found that clock genes were suppressed in B16 cells and tumors, but treatments inducing circadian rhythmicity, such as dexamethasone, forskolin and heat shock, triggered rhythmic clock and cell cycle gene expression, which resulted in fewer cells in S phase and more in G1 phase. Accordingly, B16 proliferation in vitro and tumor growth in vivo was slowed down. Similar effects were observed in human colon carcinoma HCT-116 cells. Notably, the effects of dexamethasone were not due to an increase in apoptosis nor to an enhancement of immune cell recruitment to the tumor. Knocking down the essential clock gene Bmal1 in B16 tumors prevented the effects of dexamethasone on tumor growth and cell cycle events.

conclusionsHere we demonstrated that the effects of dexamethasone on cell cycle and tumor growth are mediated by the tumor-intrinsic circadian clock. Thus, our work reveals that enhancing circadian clock function might represent a novel strategy to control cancer progression.

Indexed as

Circadian ClocksAnimalsARNTL Transcription FactorsCell CycleCell Line, TumorCell ProliferationCircadian RhythmColforsinDexamethasoneGene Expression Regulation, NeoplasticGene Knockdown TechniquesHCT116 CellsHeat-Shock ResponseHumansMelanoma, ExperimentalMice, Inbred C57BLARNTL Transcription FactorsBmal1 protein, mouseColforsinDexamethasoneCell cycle checkpointsCircadian clockClock gene expressionMelanoma cancerTumor growth

Identifiers

PMID28196531
PMCPMC5310078
OpenAlexW2588955044

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.