Evidence map›Paper›PMID 30158530›Full record

ArticleCell death & disease2018

The bHLH transcription factor DEC1 promotes thyroid cancer aggressiveness by the interplay with NOTCH1.

Cristina Gallo, Valentina Fragliasso, Benedetta Donati, Federica Torricelli, Annalisa Tameni, Simonetta Piana, Alessia Ciarrocchi

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  7. Circadian rhythm disruption and endocrine-related tumors.World journal of clinical oncology · 2024
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  12. Review
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  15. Notch signaling pathway: architecture, disease, and therapeutics.Signal transduction and targeted therapy · 2022
    Review
  16. Article
  17. Frontiers in pharmacology · 2022
    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

7 authors at 1 institution in 1 country.

Cristina GalloLaboratory of Translational Research, Azienda Unità Sanitaria Locale - IRCCS di Reggio Emilia, Reggio Emilia, 42123, Italy.
Valentina FragliassoLaboratory of Translational Research, Azienda Unità Sanitaria Locale - IRCCS di Reggio Emilia, Reggio Emilia, 42123, Italy.
Benedetta DonatiLaboratory of Translational Research, Azienda Unità Sanitaria Locale - IRCCS di Reggio Emilia, Reggio Emilia, 42123, Italy.
Federica TorricelliLaboratory of Translational Research, Azienda Unità Sanitaria Locale - IRCCS di Reggio Emilia, Reggio Emilia, 42123, Italy.
Annalisa TameniLaboratory of Translational Research, Azienda Unità Sanitaria Locale - IRCCS di Reggio Emilia, Reggio Emilia, 42123, Italy.
Simonetta PianaPathology Unit, Department of Oncology, Azienda Unità Sanitaria Locale - IRCCS di Reggio Emilia, Reggio Emilia, 42123, Italy.
Alessia CiarrocchiLaboratory of Translational Research, Azienda Unità Sanitaria Locale - IRCCS di Reggio Emilia, Reggio Emilia, 42123, Italy. Alessia.Ciarrocchi@ausl.re.it.
Azienda Sanitaria Unità Locale di Reggio Emilia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant re-activation of transcription factors occurs frequently in cancer. Recently, we found the basic helix-loop-helix transcription factors DEC1 and DEC2 significantly up-regulated in a model of highly aggressive thyroid cancer, raising the hypothesis that these factors might be part of the program driving progression of these tumors. Here, we investigated for the first time the function of DEC1 and DEC2 in thyroid cancer. Using both gain- and loss-of-function approaches, we showed that DEC1 more than DEC2 sustains progression of thyroid cancer by promoting cell growth and invasiveness. We demonstrated that DEC1 controls NOTCH1 expression and that the interplay with the NOTCH pathway is relevant for DEC1 function in thyroid cancer. We confirmed this observation in vivo showing that DEC1 expression is a specific feature of tumor cells, that this transcription factor is significantly over-expressed in all major thyroid cancer histotypes and that its expression correlated with NOTCH1 in these tumors. Finally, we performed RNA-sequencing to define the DEC1-associated gene expression profile in thyroid cancer cells and we discovered that DEC1 drives the expression of many cell cycle-related genes, uncovering a potential new function for this transcription factor in cancer.

Indexed as

Basic Helix-Loop-Helix ProteinsCell Line, TumorCell ProliferationGene Expression RegulationHumansReceptor, Notch1RNA, Small InterferingSignal TransductionThyroid NeoplasmsTranscriptional ActivationTranscription FactorsTumor Suppressor ProteinsBasic Helix-Loop-Helix ProteinsDELEC1 protein, humanNOTCH1 protein, humanReceptor, Notch1RNA, Small InterferingTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID30158530
PMCPMC6115386
OpenAlexW2889312540

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.