Evidence map›Paper›PMID 37798427›Full record

ArticleScientific reports2023

Pan-tissue mitochondrial phenotyping reveals lower OXPHOS expression and function across cancer types.

Ilya N Boykov, McLane M Montgomery, James T Hagen, Raphael T Aruleba, Kelsey L McLaughlin, Hannah S Coalson, Margaret A Nelson, Andrea S Pereyra, Jessica M Ellis, Tonya N Zeczycki and 4 more

Abstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Bayesian selection of lipidome dynamics features for a K-nearest neighbors (KNN) classifier model of tumor response in patients with advanced gastrointestinal adenocarcinoma undergoing systemic treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

14 authors.

Ilya N Boykov *Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
McLane M Montgomery *Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
James T HagenDepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Raphael T ArulebaDepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Kelsey L McLaughlinDepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Hannah S CoalsonDepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Margaret A NelsonDepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Andrea S PereyraDepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Jessica M EllisDepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Tonya N ZeczyckiDepartment of Biochemistry and Molecular Biology, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Nasreen A VohraDepartment of Surgery, Brody School of Medicine, East Carolina University, Greenville, NC, USA.
Su-Fern TanDepartment of Medicine, Division of Hematology/Oncology, University of Virginia School of Medicine, Charlottesville, VA, USA.
Myles C CabotEast Carolina Diabetes and Obesity Institute, East Carolina University, 115 Heart Drive, Greenville, NC, 27834, USA.
Kelsey H Fisher-WellmanDepartment of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA. fisherwellmank17@ecu.edu.

Funding

Tissue Repository and Animal Models CoreP01CA171983 · NCI · UNIVERSITY OF VIRGINIA · PI FISHER-WELLMAN, KELSEY H · 2013 to 2024
$19.9M
Determining the Biological Effects of Mitochondrial Acyl ToxicityR01DK125812 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI ELLIS, JESSICA M · 2020 to 2025
$2.3M
NCI NIH HHS P01 CA171983NIDDK NIH HHS DK125812NIDDK NIH HHS R01 DK125812
6 · The paper itself

Abstract

Targeting mitochondrial oxidative phosphorylation (OXPHOS) to treat cancer has been hampered due to serious side-effects potentially arising from the inability to discriminate between non-cancerous and cancerous mitochondria. Herein, comprehensive mitochondrial phenotyping was leveraged to define both the composition and function of OXPHOS across various murine cancers and compared to both matched normal tissues and other organs. When compared to both matched normal tissues, as well as high OXPHOS reliant organs like heart, intrinsic expression of the OXPHOS complexes, as well as OXPHOS flux were discovered to be consistently lower across distinct cancer types. Assuming intrinsic OXPHOS expression/function predicts OXPHOS reliance in vivo, these data suggest that pharmacologic blockade of mitochondrial OXPHOS likely compromises bioenergetic homeostasis in healthy oxidative organs prior to impacting tumor mitochondrial flux in a clinically meaningful way. Although these data caution against the use of indiscriminate mitochondrial inhibitors for cancer treatment, considerable heterogeneity was observed across cancer types with respect to both mitochondrial proteome composition and substrate-specific flux, highlighting the possibility for targeting discrete mitochondrial proteins or pathways unique to a given cancer type.

Indexed as

NeoplasmsOxidative PhosphorylationAnimalsEnergy MetabolismHumansMiceMitochondria

Identifiers

PMID37798427
PMCPMC10556099

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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.