Evidence map›Paper›PMID 23764021›Full record

ArticleBMC cancer2013

Mitochondria-targeted vitamin E analogs inhibit breast cancer cell energy metabolism and promote cell death.

Gang Cheng, Jacek Zielonka, Donna M McAllister, A Craig Mackinnon, Joy Joseph, Michael B Dwinell, Balaraman Kalyanaraman

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

71 citing papers in PubMed, 129 citations in OpenAlex.

  1. Review
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  6. Small molecule probes for peroxynitrite detection.Redox biochemistry and chemistry · 2024
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  14. Recent advances in mitochondrial diseases: From molecular insights to therapeutic perspectives.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
    Review
  15. Article
  16. Targeting Energy Metabolism in Cancer Treatment.International journal of molecular sciences · 2022
    Review
  17. Review
  18. Article
  19. Article
  20. Review

11 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Gang ChengFree Radical Research Center and Department of Biophysics, Medical College of Wisconsin, Milwaukee, WI, USA.
Jacek Zielonka
Donna M McAllister
A Craig Mackinnon
Joy Joseph
Michael B Dwinell
Balaraman Kalyanaraman
Medical College of Wisconsin · US

Funding

Role of iNOS, Nitric Oxide & Arginase in Statin-Mediated Toxicity in Cancer CellsR01CA125112 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI KALYANARAMAN, BALARAMAN · 2008 to 2012
$1.6M
Mitochondria-targeted Agents in Breast CancerR01CA152810 · NCI · MEDICAL COLLEGE OF WISCONSIN · PI KALYANARAMAN, BALARAMAN · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA125112NCI NIH HHS R01 CA152810
6 · The paper itself

Abstract

backgroundRecent research has revealed that targeting mitochondrial bioenergetic metabolism is a promising chemotherapeutic strategy. Key to successful implementation of this chemotherapeutic strategy is the use of new and improved mitochondria-targeted cationic agents that selectively inhibit energy metabolism in breast cancer cells, while exerting little or no long-term cytotoxic effect in normal cells.

methodsIn this study, we investigated the cytotoxicity and alterations in bioenergetic metabolism induced by mitochondria-targeted vitamin E analog (Mito-chromanol, Mito-ChM) and its acetylated ester analog (Mito-ChMAc). Assays of cell death, colony formation, mitochondrial bioenergetic function, intracellular ATP levels, intracellular and tissue concentrations of tested compounds, and in vivo tumor growth were performed.

resultsBoth Mito-ChM and Mito-ChMAc selectively depleted intracellular ATP and caused prolonged inhibition of ATP-linked oxygen consumption rate in breast cancer cells, but not in non-cancerous cells. These effects were significantly augmented by inhibition of glycolysis. Mito-ChM and Mito-ChMAc exhibited anti-proliferative effects and cytotoxicity in several breast cancer cells with different genetic background. Furthermore, Mito-ChM selectively accumulated in tumor tissue and inhibited tumor growth in a xenograft model of human breast cancer.

conclusionsWe conclude that mitochondria-targeted small molecular weight chromanols exhibit selective anti-proliferative effects and cytotoxicity in multiple breast cancer cells, and that esterification of the hydroxyl group in mito-chromanols is not a critical requirement for its anti-proliferative and cytotoxic effect.

Indexed as

AnimalsBreast NeoplasmsCell DeathCell Line, TumorChromansChromatography, High Pressure LiquidEnergy MetabolismFemaleHumansMiceMitochondriaVitamin EXenograft Model Antitumor Assays2,2,5,7,8-pentamethyl-1-hydroxychromanChromansVitamin E

Identifiers

PMID23764021
PMCPMC3686663
OpenAlexW2161859769

What OpenQuestion holds

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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.