Evidence map›Paper›PMID 30723235›Full record

ArticleScientific reports2019

SIX1 represses senescence and promotes SOX2-mediated cellular plasticity during tumorigenesis.

Cristina De Lope, Samara Martín-Alonso, Jaione Auzmendi-Iriarte, Carmen Escudero, Isabel Mulet, Javier Larrasa-Alonso, Irene López-Antona, Ander Matheu, Ignacio Palmero

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  6. SIX1 Downregulation Suppresses Self-renewal Capacity and THY1 Expression in Hepatocellular Carcinoma and SIX1 Dominate the Survival in Liver Cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2023
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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

9 authors at 4 institutions in 1 country.

Cristina De LopeInstituto de Investigaciones Biomédicas "Alberto Sols" CSIC-UAM, Madrid, Spain.
Samara Martín-AlonsoInstituto de Investigaciones Biomédicas "Alberto Sols" CSIC-UAM, Madrid, Spain.
Jaione Auzmendi-IriarteInstituto de Investigación Sanitaria Biodonostia, San Sebastián, Spain.
Carmen EscuderoInstituto de Investigaciones Biomédicas "Alberto Sols" CSIC-UAM, Madrid, Spain.
Isabel MuletInstituto de Investigaciones Biomédicas "Alberto Sols" CSIC-UAM, Madrid, Spain.
Javier Larrasa-AlonsoInstituto de Investigaciones Biomédicas "Alberto Sols" CSIC-UAM, Madrid, Spain.
Irene López-AntonaInstituto de Investigaciones Biomédicas "Alberto Sols" CSIC-UAM, Madrid, Spain.
Ander MatheuInstituto de Investigación Sanitaria Biodonostia, San Sebastián, Spain.
Ignacio PalmeroInstituto de Investigaciones Biomédicas "Alberto Sols" CSIC-UAM, Madrid, Spain. ipalmero@iib.uam.es.
Instituto de Investigaciones Biomédicas Sols-Morreale · ESBiogipuzkoa Health Research Institute · ESSpanish National Centre for Cardiovascular Research · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Six1 is a developmental transcriptional regulator frequently overexpressed in human tumors. Recent results show that SIX1 also acts as a repressor of cell senescence, an antiproliferative response with a key role in tumor suppression, among other physiological and pathological settings. Here, we set to study the impact of SIX1 gain of function in transformation and tumorigenesis of fibroblasts, in connection with senescence. Using transcriptomic, histological, and functional analyses in murine tumors and cells of fibroblast origin, we show that SIX1 has a strong pro-tumorigenic action in this model, linked to the repression of a senescence-related gene signature and the induction of an undifferentiated phenotype mediated, at least in part, by the regulation of the stemness factor Sox2. Moreover, functional analyses with human glioma cell lines also show that SIX1 controls SOX2 expression, senescence and self-renewal in this model. Collectively, our results support a general link of SIX1 with senescence and SOX2-mediated cell plasticity in tumors.

Indexed as

AnimalsBrain NeoplasmsCarcinogenesisCell Line, TumorCell PlasticityCellular SenescenceFemaleFibroblastsGene Expression Regulation, NeoplasticGliomaHeterograftsHomeodomain ProteinsHumansMiceMice, NudeSOXB1 Transcription FactorsHomeodomain ProteinsSIX1 protein, humanSix1 protein, mouseSOX2 protein, humanSox2 protein, mouseSOXB1 Transcription Factors

Identifiers

PMID30723235
PMCPMC6363751
OpenAlexW2912316011

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.