Evidence map›Paper›PMID 35628366›Full record

ArticleInternational journal of molecular sciences2022

Involvement of ORAI1/SOCE in Human AML Cell Lines and Primary Cells According to ABCB1 Activity, LSC Compartment and Potential Resistance to Ara-C Exposure.

Clara Lewuillon, Aurélie Guillemette, Sofia Titah, Faruk Azam Shaik, Nathalie Jouy, Ossama Labiad, Valerio Farfariello, Marie-Océane Laguillaumie, Thierry Idziorek, Adeline Barthélémy and 7 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 10 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

17 authors at 4 institutions in 2 countries.

Clara LewuillonCNRS, Inserm, CHU Lille, UMR 9020, UMR-S 1277-Canther-Cancer Heterogeneity, Plasticity and Resistance to Therapies, Université de Lille, F-59000 Lille, France.ORCID 0000-0002-8594-032X
Aurélie GuillemetteCNRS, Inserm, CHU Lille, UMR 9020, UMR-S 1277-Canther-Cancer Heterogeneity, Plasticity and Resistance to Therapies, Université de Lille, F-59000 Lille, France.ORCID 0000-0002-3422-3689
Sofia TitahCNRS, Inserm, CHU Lille, UMR 9020, UMR-S 1277-Canther-Cancer Heterogeneity, Plasticity and Resistance to Therapies, Université de Lille, F-59000 Lille, France.ORCID 0000-0003-4892-6817
Faruk Azam ShaikInstitut de Recherche sur le Cancer de Lille (IRCL), F-59000 Lille, France.ORCID 0000-0002-9449-5168
Nathalie JouyUMS 2014/US41 Plateformes Lilloises En Biologie Et Sante, Université de Lille, F-59000 Lille, France.
Ossama LabiadCNRS, Inserm, CHU Lille, UMR 9020, UMR-S 1277-Canther-Cancer Heterogeneity, Plasticity and Resistance to Therapies, Université de Lille, F-59000 Lille, France.
Valerio FarfarielloInserm, U1003-PHYCEL-Physiologie Cellulaire, Université de Lille, F-59000 Lille, France.
Marie-Océane LaguillaumieCNRS, Inserm, CHU Lille, UMR 9020, UMR-S 1277-Canther-Cancer Heterogeneity, Plasticity and Resistance to Therapies, Université de Lille, F-59000 Lille, France.ORCID 0000-0002-4870-5435
Thierry IdziorekCNRS, Inserm, CHU Lille, UMR 9020, UMR-S 1277-Canther-Cancer Heterogeneity, Plasticity and Resistance to Therapies, Université de Lille, F-59000 Lille, France.ORCID 0000-0001-5893-9131
Adeline BarthélémyCNRS, Inserm, CHU Lille, UMR 9020, UMR-S 1277-Canther-Cancer Heterogeneity, Plasticity and Resistance to Therapies, Université de Lille, F-59000 Lille, France.
Pauline PeyrouzeCNRS, Inserm, CHU Lille, UMR 9020, UMR-S 1277-Canther-Cancer Heterogeneity, Plasticity and Resistance to Therapies, Université de Lille, F-59000 Lille, France.
Céline BerthonCNRS, Inserm, CHU Lille, UMR 9020, UMR-S 1277-Canther-Cancer Heterogeneity, Plasticity and Resistance to Therapies, Université de Lille, F-59000 Lille, France.
Mehmet Cagatay TarhanLIMMS/CNRS-IIS IRL2820, The University of Tokyo, Tokyo 153-8505, Japan.
Meyling CheokCNRS, Inserm, CHU Lille, UMR 9020, UMR-S 1277-Canther-Cancer Heterogeneity, Plasticity and Resistance to Therapies, Université de Lille, F-59000 Lille, France.ORCID 0000-0002-7820-8026
Bruno QuesnelCNRS, Inserm, CHU Lille, UMR 9020, UMR-S 1277-Canther-Cancer Heterogeneity, Plasticity and Resistance to Therapies, Université de Lille, F-59000 Lille, France.ORCID 0000-0002-6563-2709
Loïc LemonnierInserm, U1003-PHYCEL-Physiologie Cellulaire, Université de Lille, F-59000 Lille, France.ORCID 0000-0001-6200-5382
Yasmine TouilCNRS, Inserm, CHU Lille, UMR 9020, UMR-S 1277-Canther-Cancer Heterogeneity, Plasticity and Resistance to Therapies, Université de Lille, F-59000 Lille, France.ORCID 0000-0002-2286-960X
Centre National de la Recherche Scientifique · FRInserm · FRLaboratory for Integrated Micro-Mechatronic Systems · JPUniversité de Lille · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a hematological malignancy with a high risk of relapse. This issue is associated with the development of mechanisms leading to drug resistance that are not yet fully understood. In this context, we previously showed the clinical significance of the ATP binding cassette subfamily B-member 1 (ABCB1) in AML patients, namely its association with stemness markers and an overall worth prognosis. Calcium signaling dysregulations affect numerous cellular functions and are associated with the development of the hallmarks of cancer. However, in AML, calcium-dependent signaling pathways remain poorly investigated. With this study, we show the involvement of the ORAI1 calcium channel in store-operated calcium entry (SOCE), the main calcium entry pathway in non-excitable cells, in two representative human AML cell lines (KG1 and U937) and in primary cells isolated from patients. Moreover, our data suggest that in these models, SOCE varies according to the differentiation status, ABCB1 activity level and leukemic stem cell (LSC) proportion. Finally, we present evidence that ORAI1 expression and SOCE amplitude are modulated during the establishment of an apoptosis resistance phenotype elicited by the chemotherapeutic drug Ara-C. Our results therefore suggest ORAI1/SOCE as potential markers of AML progression and drug resistance apparition.

Indexed as

CytarabineLeukemia, Myeloid, AcuteATP Binding Cassette Transporter, Subfamily BCalciumCalcium SignalingCell LineHumansORAI1 ProteinStromal Interaction Molecule 1ABCB1 protein, humanATP Binding Cassette Transporter, Subfamily BCalciumCytarabineORAI1 ProteinORAI1 protein, humanStromal Interaction Molecule 1ABCB1AMLAra-Ccalciumleukemic stem cellsNFATORAI1SOCE

Identifiers

PMID35628366
PMCPMC9141756
OpenAlexW4280581138

What Socratic 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 Socratic graph.