Mitochondrial Metabolism as a Target for Cancer Therapy

Recent evidence in humans and mice supports the notion that mitochondrial metabolism is active and necessary for tumor growth. Mitochondrial metabolism supports tumor anabolism by providing key metabolites for macromolecule synthesis and generating oncometabolites to maintain the cancer phenotype. M...

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Published inCell metabolism Vol. 32; no. 3; pp. 341 - 352
Main Authors Vasan, Karthik, Werner, Marie, Chandel, Navdeep S.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.09.2020
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Abstract Recent evidence in humans and mice supports the notion that mitochondrial metabolism is active and necessary for tumor growth. Mitochondrial metabolism supports tumor anabolism by providing key metabolites for macromolecule synthesis and generating oncometabolites to maintain the cancer phenotype. Moreover, there are multiple clinical trials testing the efficacy of inhibiting mitochondrial metabolism as a new cancer therapeutic treatment. In this review, we discuss the rationale of using these anti-cancer agents in clinical trials and highlight how to effectively utilize them in different tumor contexts. Recent evidence indicates that mitochondrial metabolism is essential for tumorigenesis. Vasan et al. review multiple mitochondrial drugs in clinical trials for various cancers, including metformin. Also, they report a genetic screen highlighting mechanisms of resistance to metformin.
AbstractList Recent evidence in humans and mice supports the notion that mitochondrial metabolism is active and necessary for tumor growth. Mitochondrial metabolism supports tumor anabolism by providing key metabolites for macromolecule synthesis and generating oncometabolites to maintain the cancer phenotype. Moreover, there are multiple clinical trials testing the efficacy of inhibiting mitochondrial metabolism as a new cancer therapeutic treatment. In this review, we discuss the rationale of using these anti-cancer agents in clinical trials and highlight how to effectively utilize them in different tumor contexts.Recent evidence in humans and mice supports the notion that mitochondrial metabolism is active and necessary for tumor growth. Mitochondrial metabolism supports tumor anabolism by providing key metabolites for macromolecule synthesis and generating oncometabolites to maintain the cancer phenotype. Moreover, there are multiple clinical trials testing the efficacy of inhibiting mitochondrial metabolism as a new cancer therapeutic treatment. In this review, we discuss the rationale of using these anti-cancer agents in clinical trials and highlight how to effectively utilize them in different tumor contexts.
Recent evidence in humans and mice supports the notion that mitochondrial metabolism is active and necessary for tumor growth. Mitochondrial metabolism supports tumor anabolism by providing key metabolites for macromolecule synthesis and generating oncometabolites to maintain the cancer phenotype. Moreover, there are multiple clinical trials testing the efficacy of inhibiting mitochondrial metabolism as a new cancer therapeutic treatment. In this review, we discuss the rationale of using these anti-cancer agents in clinical trials and highlight how to effectively utilize them in different tumor contexts. Recent evidence indicates that mitochondrial metabolism is essential for tumorigenesis. Vasan et al. review multiple mitochondrial drugs in clinical trials for various cancers, including metformin. Also, they report a genetic screen highlighting mechanisms of resistance to metformin.
Recent evidence in humans and mice supports the notion that mitochondrial metabolism is active and necessary for tumor growth. Mitochondrial metabolism supports tumor anabolism by providing key metabolites for macromolecule synthesis and generating oncometabolites to maintain the cancer phenotype. Moreover, there are multiple clinical trials testing the efficacy of inhibiting mitochondrial metabolism as a new cancer therapeutic treatment. In this review, we discuss the rationale of using these anti-cancer agents in clinical trials and highlight how to effectively utilize them in different tumor contexts.
Author Vasan, Karthik
Chandel, Navdeep S.
Werner, Marie
AuthorAffiliation 1 Department of Medicine, Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
AuthorAffiliation_xml – name: 1 Department of Medicine, Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
Author_xml – sequence: 1
  givenname: Karthik
  surname: Vasan
  fullname: Vasan, Karthik
  organization: Department of Medicine, Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
– sequence: 2
  givenname: Marie
  surname: Werner
  fullname: Werner, Marie
  organization: Department of Medicine, Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
– sequence: 3
  givenname: Navdeep S.
  surname: Chandel
  fullname: Chandel, Navdeep S.
  email: nav@northwestern.edu
  organization: Department of Medicine, Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32668195$$D View this record in MEDLINE/PubMed
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Snippet Recent evidence in humans and mice supports the notion that mitochondrial metabolism is active and necessary for tumor growth. Mitochondrial metabolism...
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SubjectTerms Animals
Antineoplastic Agents - chemistry
Antineoplastic Agents - pharmacology
Humans
metformin
mitochondria
Mitochondria - drug effects
Mitochondria - metabolism
Neoplasms - drug therapy
Neoplasms - metabolism
Title Mitochondrial Metabolism as a Target for Cancer Therapy
URI https://dx.doi.org/10.1016/j.cmet.2020.06.019
https://www.ncbi.nlm.nih.gov/pubmed/32668195
https://www.proquest.com/docview/2424442765
https://pubmed.ncbi.nlm.nih.gov/PMC7483781
Volume 32
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