Evidence map›Paper›PMID 34496224›Full record

ArticleFree radical biology & medicine2021

Loss of the redox mitochondrial protein mitoNEET leads to mitochondrial dysfunction in B-cell acute lymphoblastic leukemia.

Werner J Geldenhuys, Debbie Piktel, Javohn C Moore, Stephanie L Rellick, Ethan Meadows, Mark V Pinti, John M Hollander, Amanda G Ammer, Karen H Martin, Laura F Gibson

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  9. Structure and biological evaluation ofAdvances in redox research · 2022
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  11. Review
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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 1 institution in 1 country.

Werner J GeldenhuysDepartment of Pharmaceutical Sciences, West Virginia University School of Pharmacy, Morgantown, WV, USA; Mitochondria Metabolism and Bioenergetics Working Group, West Virginia University School of Medicine, Morgantown, WV, USA.
Debbie PiktelDepartment of Microbiology, Immunology and Cell Biology, West Virginia University School of Medicine, Morgantown, WV, USA; West Virginia University Cancer Institute, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV, USA.
Javohn C MooreWest Virginia University Cancer Institute, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV, USA.
Stephanie L RellickWest Virginia University Cancer Institute, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV, USA.
Ethan MeadowsDepartment of Human Performance, West Virginia University School of Medicine, Morgantown, WV, USA; Mitochondria Metabolism and Bioenergetics Working Group, West Virginia University School of Medicine, Morgantown, WV, USA.
Mark V PintiDepartment of Human Performance, West Virginia University School of Medicine, Morgantown, WV, USA; Mitochondria Metabolism and Bioenergetics Working Group, West Virginia University School of Medicine, Morgantown, WV, USA.
John M HollanderDepartment of Human Performance, West Virginia University School of Medicine, Morgantown, WV, USA; Mitochondria Metabolism and Bioenergetics Working Group, West Virginia University School of Medicine, Morgantown, WV, USA.
Amanda G AmmerWest Virginia University Cancer Institute, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV, USA.
Karen H MartinDepartment of Microbiology, Immunology and Cell Biology, West Virginia University School of Medicine, Morgantown, WV, USA; West Virginia University Cancer Institute, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV, USA.
Laura F GibsonDepartment of Microbiology, Immunology and Cell Biology, West Virginia University School of Medicine, Morgantown, WV, USA; West Virginia University Cancer Institute, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV, USA. Electronic address: lgibson@hsc.wvu.edu.
West Virginia University · US

Funding

West Virginia IDEA-CTRU54GM104942 · NIGMS · WEST VIRGINIA UNIVERSITY · PI Sally Lynn Hodder · 2012 to 2026
$81.0M
WV INBRE: The Inhibitor of Growth Family Member 4 (ING4) inhibits L-Type Amino Acid Transporter 1 (LAT1) expression to suppress Breast CancerP20GM103434 · NIGMS · MARSHALL UNIVERSITY · PI GARY O RANKIN · 2012 to 2026
$61.1M
West Virginia University Stroke COBREP20GM109098 · NIGMS · WEST VIRGINIA UNIVERSITY · PI DEVRIES, ANNE COURTNEY · 2014 to 2024
$24.5M
THE ROLE OF HEF1 PROTEIN IN INVASION OF METASTATIC BREAST CANCERP20RR016440 · NCRR · WEST VIRGINIA UNIVERSITY · PI CUFF, CHRISTOPHER F · 2001 to 2010
$22.8M
WVU Flow Cytometry and Single Cell Core Facility (FCSCCF)P20GM121322 · NIGMS · WEST VIRGINIA UNIVERSITY · PI William Harry Walker · 2018 to 2026
$22.4M
West Virginia Flow Cytometry Core FacilityP30GM103488 · NIGMS · WEST VIRGINIA UNIVERSITY · PI CUFF, CHRISTOPHER F · 2012 to 2016
$4.8M
miRNA Regulation of the Mitochondrial GenomeR01HL128485 · NHLBI · WEST VIRGINIA UNIVERSITY · PI HOLLANDER, JOHN M · 2017 to 2019
$1.3M
miRNA Regulation of the Mitochondrial GenomeR56HL128485 · NHLBI · WEST VIRGINIA UNIVERSITY · PI HOLLANDER, JOHN M · 2015 to 2015
$410k
Special Becton Dickinson Fortessa Flow CytometerS10OD016165 · OD · WEST VIRGINIA UNIVERSITY · PI CUFF, CHRISTOPHER F · 2013 to 2013
$384k
NCRR NIH HHS P20 RR016440NHLBI NIH HHS R01 HL128485NHLBI NIH HHS R56 HL128485NIGMS NIH HHS P20 GM103434NIGMS NIH HHS P20 GM109098NIGMS NIH HHS P20 GM121322NIGMS NIH HHS P30 GM103488NIGMS NIH HHS U54 GM104942NIH HHS S10 OD016165
6 · The paper itself

Abstract

B-cell acute lymphoblastic leukemia (ALL) affects both pediatric and adult patients. Chemotherapy resistant tumor cells that contribute to minimal residual disease (MRD) underlie relapse and poor clinical outcomes in a sub-set of patients. Targeting mitochondrial oxidative phosphorylation (OXPHOS) in the treatment of refractory leukemic cells is a potential novel approach to sensitizing tumor cells to existing standard of care therapeutic agents. In the current study, we have expanded our previous investigation of the mitoNEET ligand NL-1 in the treatment of ALL to interrogate the functional role of the mitochondrial outer membrane protein mitoNEET in B-cell ALL. Knockout (KO) of mitoNEET (gene: CISD1) in REH leukemic cells led to changes in mitochondrial ultra-structure and function. REH cells have significantly reduced OXPHOS capacity in the KO cells coincident with reduction in electron flow and increased reactive oxygen species. In addition, we found a decrease in lipid content in KO cells, as compared to the vector control cells was observed. Lastly, the KO of mitoNEET was associated with decreased proliferation as compared to control cells when exposed to the standard of care agent cytarabine (Ara-C). Taken together, these observations suggest that mitoNEET is essential for optimal function of mitochondria in B-cell ALL and may represent a novel anti-leukemic drug target for treatment of minimal residual disease.

Indexed as

Mitochondrial ProteinsPrecursor Cell Lymphoblastic Leukemia-LymphomaB-LymphocytesChildHumansMitochondriaOxidation-ReductionMitochondrial ProteinsChemoresistancecisd2GlitazonesMitochondrial dysfunction

Identifiers

PMID34496224
PMCPMC8478879
OpenAlexW3198087653

What OpenQuestion holds

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Registered trials

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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.