Evidence map›Paper›PMID 32432042›Full record

ArticleFrontiers in oncology2020

FtH-Mediated ROS Dysregulation Promotes CXCL12/CXCR4 Axis Activation and EMT-Like Trans-Differentiation in Erythroleukemia K562 Cells.

Roberta Chirillo, Ilenia Aversa, Anna Di Vito, Alessandro Salatino, Anna Martina Battaglia, Alessandro Sacco, Maddalena Adriana Di Sanzo, Maria Concetta Faniello, Barbara Quaresima, Camillo Palmieri and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

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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

12 authors at 1 institution in 1 country.

Roberta ChirilloDepartment of Experimental and Clinical Medicine, "Magna Græcia" University of Catanzaro, Catanzaro, Italy.
Ilenia AversaDepartment of Experimental and Clinical Medicine, "Magna Græcia" University of Catanzaro, Catanzaro, Italy.
Anna Di VitoDepartment of Experimental and Clinical Medicine, "Magna Græcia" University of Catanzaro, Catanzaro, Italy.
Alessandro SalatinoDepartment of Experimental and Clinical Medicine, "Magna Græcia" University of Catanzaro, Catanzaro, Italy.
Anna Martina BattagliaDepartment of Experimental and Clinical Medicine, "Magna Græcia" University of Catanzaro, Catanzaro, Italy.
Alessandro SaccoDepartment of Experimental and Clinical Medicine, "Magna Græcia" University of Catanzaro, Catanzaro, Italy.
Maddalena Adriana Di SanzoDepartment of Experimental and Clinical Medicine, "Magna Græcia" University of Catanzaro, Catanzaro, Italy.
Maria Concetta FanielloDepartment of Experimental and Clinical Medicine, "Magna Græcia" University of Catanzaro, Catanzaro, Italy.
Barbara QuaresimaDepartment of Experimental and Clinical Medicine, "Magna Græcia" University of Catanzaro, Catanzaro, Italy.
Camillo PalmieriDepartment of Experimental and Clinical Medicine, "Magna Græcia" University of Catanzaro, Catanzaro, Italy.
Flavia BiamonteDepartment of Experimental and Clinical Medicine, "Magna Græcia" University of Catanzaro, Catanzaro, Italy.
Francesco CostanzoDepartment of Experimental and Clinical Medicine, Research Center of Biochemistry and Advanced Molecular Biology, "Magna Græcia" University of Catanzaro, Catanzaro, Italy.
Magna Graecia University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cell-microenvironment communication is essential for homing of hematopoietic stem cells in stromal niches. Recent evidences support the involvement of epithelial-to-mesenchymal (EMT) process in hematopoietic stem cell homeostasis as well as in leukemia cells invasiveness and migration capability. Here, we demonstrate that the alteration of iron homeostasis and the consequent increase of redox metabolism, mediated by the stable knock down of ferritin heavy chain (FtH), enhances the expression of CXCR4 in K562 erythroleukemia cells, thus promoting CXCL12-mediated motility. Indeed, addition of the CXCR4 receptor antagonist AMD3100 reverts this effect. Upon FtH knock down K562 cells also acquire an "EMT-like" phenotype, characterized by the increase of

Indexed as

CXCR4EMTferritin heavy chainhematological malignanciesleukemiaNF-κBROStumor microenvironment

Identifiers

PMID32432042
PMCPMC7214836
OpenAlexW3023956837

What OpenQuestion holds

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LicenceCC BY
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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.