Evidence map›Paper›PMID 34282187›Full record

ArticleScientific reports2021

The role of FOSL1 in stem-like cell reprogramming processes.

Valeria Pecce, Antonella Verrienti, Giulia Fiscon, Marialuisa Sponziello, Federica Conte, Luana Abballe, Cosimo Durante, Lorenzo Farina, Sebastiano Filetti, Paola Paci

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.5field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 50 citations in OpenAlex.

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  19. FOSL1 promotes proneural-to-mesenchymal transition of glioblastoma stem cells via UBC9/CYLD/NF-κB axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
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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

10 authors at 5 institutions in 1 country.

Valeria PecceDepartment of Translational and Precision Medicine, Sapienza University of Rome, 00161, Rome, Italy. valeria.pecce@uniroma1.it.
Antonella VerrientiDepartment of Translational and Precision Medicine, Sapienza University of Rome, 00161, Rome, Italy.
Giulia FisconFondazione Per La Medicina Personalizzata, Via Goffredo Mameli, 3/1, Genoa, Italy.
Marialuisa SponzielloDepartment of Translational and Precision Medicine, Sapienza University of Rome, 00161, Rome, Italy.
Federica ConteInstitute for Systems Analysis and Computer Science "Antonio Ruberti", National Research Council, Rome, Italy.
Luana AbballeDepartment of Pediatric Hematology/Oncology and Cell and Gene Therapy, IRCCS, Ospedale Pediatrico Bambino Gesù, Piazza Sant'Onofrio 4, 00165, Rome, Italy.
Cosimo DuranteDepartment of Translational and Precision Medicine, Sapienza University of Rome, 00161, Rome, Italy.
Lorenzo FarinaDepartment of Computer, Control, and Management Engineering, Sapienza University of Rome, Rome, Italy.
Sebastiano FilettiSchool of Health, Unitelma Sapienza University of Rome, Rome, Italy.
Paola PaciInstitute for Systems Analysis and Computer Science "Antonio Ruberti", National Research Council, Rome, Italy.
Sapienza University of Rome · ITNational Research Council · ITBambino Gesù Children's Hospital · ITGruppo Italiano per lo Studio dei Carcinomi dell’Apparato Digerente · ITUnitelma Sapienza University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stem-like cells (CSCs) have self-renewal abilities responsible for cancer progression, therapy resistance, and metastatic growth. The glioblastoma stem-like cells are the most studied among CSC populations. A recent study identified four transcription factors (SOX2, SALL2, OLIG2, and POU3F2) as the minimal core sufficient to reprogram differentiated glioblastoma (GBM) cells into stem-like cells. Transcriptomic data of GBM tissues and cell lines from two different datasets were then analyzed by the SWItch Miner (SWIM), a network-based software, and FOSL1 was identified as a putative regulator of the previously identified minimal core. Herein, we selected NTERA-2 and HEK293T cells to perform an in vitro study to investigate the role of FOSL1 in the reprogramming mechanisms. We transfected the two cell lines with a constitutive FOSL1 cDNA plasmid. We demonstrated that FOSL1 directly regulates the four transcription factors binding their promoter regions, is involved in the deregulation of several stemness markers, and reduces the cells' ability to generate aggregates increasing the extracellular matrix component FN1. Although further experiments are necessary, our data suggest that FOSL1 reprograms the stemness by regulating the core of the four transcription factors.

Indexed as

Brain NeoplasmsCell DifferentiationCell Line, TumorCellular ReprogrammingFos-Related Antigen 1Gene Expression Regulation, NeoplasticGlioblastomaHEK293 CellsHeLa CellsHumansNeoplastic Stem CellsProto-Oncogene Proteins c-fosFos-Related Antigen 1Proto-Oncogene Proteins c-fos

Identifiers

PMID34282187
PMCPMC8290037
OpenAlexW3184430035

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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.