Evidence map›Paper›PMID 32816185›Full record

ArticleClinical & experimental metastasis2020

Cancer stem cell generation during epithelial-mesenchymal transition is temporally gated by intrinsic circadian clocks.

Arpan De, Dilshan H Beligala, Vishal P Sharma, Christian A Burgos, Angelia M Lee, Michael E Geusz

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical & experimental metastasis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 50 citations in OpenAlex.

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  9. Tumor circadian clock strength influences metastatic potential and predicts patient prognosis in luminal A breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  10. Biological clock regulation by theFrontiers in cell and developmental biology · 2024
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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

6 authors at 3 institutions in 2 countries.

Arpan DeDepartment of Biological Sciences, Bowling Green State University, 217 Life Science Bldg., Bowling Green, OH, 43403, USA.ORCID https://orcid.org/0000-0001-8237-6703
Dilshan H BeligalaDepartment of Biological Sciences, Bowling Green State University, 217 Life Science Bldg., Bowling Green, OH, 43403, USA.
Vishal P SharmaDepartment of Biological Sciences, Bowling Green State University, 217 Life Science Bldg., Bowling Green, OH, 43403, USA.
Christian A BurgosDepartment of Biological Sciences, Bowling Green State University, 217 Life Science Bldg., Bowling Green, OH, 43403, USA.
Angelia M LeeDepartment of Biological Sciences, Bowling Green State University, 217 Life Science Bldg., Bowling Green, OH, 43403, USA.
Michael E GeuszDepartment of Biological Sciences, Bowling Green State University, 217 Life Science Bldg., Bowling Green, OH, 43403, USA. mgeusz@bgsu.edu.
Bowling Green State University · USThe University of Texas MD Anderson Cancer Center · USUniversity of Peradeniya · LK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is a key event preceding tumor cell metastasis that increases cell invasiveness and cancer stem cell (CSC) populations. Studies suggest that genes used in generating circadian rhythms also serve in regulating EMT. To test the role of circadian clocks in cellular EMT events two cancer cell lines were compared, one that has a well-established circadian clock, C6 from rat glioma, and one that does not, MCF-7 from human breast tumor. MCF-7 tumorsphere cultures were tested for evidence of circadian rhythms because of previously reported circadian rhythm enhancement in C6 tumorspheres shown by elevated rhythm amplitude and increased expression of circadian clock gene Per2. Bioluminescence imaging of Per2 gene expression in MCF-7 tumorspheres revealed a previously unconfirmed circadian clock in this important cancer research model. Inducing CSC generation through EMT in C6 and MCF-7 monolayer cultures revealed circadian oscillations in the size of the post-EMT CSC population, confirming that circadian rhythms are additional processes controlling this stage of cancer progression. EMT was verified by distinct cellular morphological changes and expression of stem cell proteins OCT4, nestin, MSI1, and CD133 along with EMT-related proteins ZEB1, vimentin, and TWIST. Quantifying single-cell events and behaviors through time-lapse imaging indicated the post-EMT population size was determined largely by circadian rhythms in epithelial-like cancer cells undergoing EMT. We then identified a specific phase of the circadian rhythm in Per2 gene activation as a potential target for therapeutic treatments that may suppress EMT, minimize CSCs, and limit metastasis.

Indexed as

Circadian ClocksEpithelial-Mesenchymal TransitionAnimalsBiomarkersBreast NeoplasmsCell MovementCell ProliferationFemaleGliomaHumansNeoplastic Stem CellsRatsSpheroids, CellularTumor Cells, CulturedBiomarkersCancer stem cellCircadian rhythmEpithelial-mesenchymal transitionOCT4Tumorsphere

Identifiers

PMID32816185
OpenAlexW3064492552

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.