Evidence map›Paper›PMID 32667731›Full record

ArticleJournal of cellular and molecular medicine2020

Acriflavine targets oncogenic STAT5 signaling in myeloid leukemia cells.

Rawan Hallal, Rawan Nehme, Marie Brachet-Botineau, Ali Nehme, Hassan Dakik, Margaux Deynoux, Persio Dello Sbarba, Yves Levern, Kazem Zibara, Fabrice Gouilleux and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

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  10. Acriflavine targets oncogenic STAT5 signaling in myeloid leukemia cells.Journal of cellular and molecular medicine · 2020
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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

11 authors at 3 institutions in 3 countries.

Rawan HallalUniversité de Tours, EA7501 GICC, Tours, France.
Rawan NehmeUniversité de Tours, EA7501 GICC, Tours, France.
Marie Brachet-BotineauUniversité de Tours, EA7501 GICC, Tours, France.
Ali NehmeUniversité de Tours, EA7501 GICC, Tours, France.
Hassan DakikUniversité de Tours, EA7501 GICC, Tours, France.
Margaux DeynouxUniversité de Tours, EA7501 GICC, Tours, France.
Persio Dello SbarbaDipartimento di Scienze Biomediche Sperimentali e Cliniche "Mario Serio", Università degli Studi di Firenze, Florence, Italy.
Yves LevernINRAE, Imagerie en Infectiologie, UMR Infectiologie et Santé Publique, Université de Tours, Nouzilly, France.
Kazem ZibaraPRASE, Lebanese University, Beirut, Lebanon.
Fabrice GouilleuxUniversité de Tours, EA7501 GICC, Tours, France.ORCID 0000-0001-6047-1718
Frédéric MazurierUniversité de Tours, EA7501 GICC, Tours, France.ORCID 0000-0002-6984-7096
Université de Tours · FRLebanese University · LBUniversity of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acriflavine (ACF) is an antiseptic with anticancer properties, blocking the growth of solid and haematopoietic tumour cells. Moreover, this compound has been also shown to overcome the resistance of cancer cells to chemotherapeutic agents. ACF has been shown to target hypoxia-inducible factors (HIFs) activity, which are key effectors of hypoxia-mediated chemoresistance. In this study, we showed that ACF inhibits the growth and survival of chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML) cell lines in normoxic conditions. We further demonstrated that ACF down-regulates STAT5 expression in CML and AML cells but activates STAT3 in CML cells in a HIF-independent manner. In addition, we demonstrated that ACF suppresses the resistance of CML cells to tyrosine kinase inhibitors, such as imatinib. Our data suggest that the dual effect of ACF might be exploited to eradicate de novo or acquired resistance of myeloid leukaemia cells to chemotherapy.

Indexed as

AcriflavineAntineoplastic AgentsCarcinogenesisCell Line, TumorCell ProliferationDown-RegulationDrug Resistance, NeoplasmHumansK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveProtein Kinase InhibitorsSignal TransductionSTAT5 Transcription FactorTumor Suppressor ProteinsAcriflavineAntineoplastic AgentsProtein Kinase InhibitorsSTAT5A protein, humanSTAT5 Transcription FactorTumor Suppressor Proteinsacriflavineapoptosiscell cyclechronic myeloid leukaemiaresistanceSTAT5

Identifiers

PMID32667731
PMCPMC7520299
OpenAlexW3043434955

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.