Fatty acid oxidation: An emerging facet of metabolic transformation in cancer

Cancer cells undergo metabolic reprogramming such as enhanced aerobic glycolysis, mutations in the tricarboxylic acid cycle enzymes, and upregulation of de novo lipid synthesis and glutaminolysis. These alterations are pivotal to the development and maintenance of the malignant phenotype of cancer c...

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Veröffentlicht in:	Cancer letters Jg. 435; S. 92 - 100
Hauptverfasser:	Ma, Yibao, Temkin, Sarah M., Hawkridge, Adam M., Guo, Chunqing, Wang, Wei, Wang, Xiang-Yang, Fang, Xianjun
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	Ireland Elsevier B.V 28.10.2018 Elsevier Limited
Schlagworte:	Angina pectoris Apoptosis ATP Biosynthesis Breast cancer Cancer Cell growth Cell proliferation Cell Transformation, Neoplastic - metabolism Dehydrogenases Drug resistance Energy Metabolism Enzymes Fatty acid β-oxidation Fatty acids Fatty Acids - metabolism Genetic transformation Glycolysis Humans Kinases Leukemia Lipid Metabolism Lipolysis Lipolytic phenotype Medical research Medicine Metabolic pathways Metabolism Metastases Metastasis Mitochondria Mitochondria - metabolism NADPH Neoplasms - metabolism Neoplasms - pathology NMR Nuclear magnetic resonance Oxidation Oxidation-Reduction Phenotypes Prostate cancer Transgenic animals Tricarboxylic acid cycle Tumor Microenvironment Tumorigenesis Asia Europe NADPH Fatty acid β-oxidation ATP Lipolytic phenotype Cancer
ISSN:	0304-3835, 1872-7980, 1872-7980
Online-Zugang:	Volltext
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Abstract	Cancer cells undergo metabolic reprogramming such as enhanced aerobic glycolysis, mutations in the tricarboxylic acid cycle enzymes, and upregulation of de novo lipid synthesis and glutaminolysis. These alterations are pivotal to the development and maintenance of the malignant phenotype of cancer cells in unfavorable tumor microenvironment or metastatic sites. Although mitochondrial fatty acid β-oxidation (FAO) is a primary bioenergetic source, it has not been generally recognized as part of the metabolic landscape of cancer. The last few years, however, have seen a dramatic change in the view of cancer relevance of the FAO pathway. Many recent studies have provided significant evidence to support a “lipolytic phenotype” of cancer. FAO, like other well-defined metabolic pathways involved in cancer, is dysregulated in diverse human malignancies. Cancer cells rely on FAO for proliferation, survival, stemness, drug resistance, and metastatic progression. FAO is also reprogrammed in cancer-associated immune and other host cells, which may contribute to immune suppression and tumor-promoting microenvironment. This article reviews and puts into context our current understanding of multi-faceted roles of FAO in oncogenesis as well as anti-cancer therapeutic opportunities posed by the FAO pathway. •FAO emerges as a new aspect of metabolic transformation in cancer.•Cancer cells rely on FAO for growth, stemness, drug resistance and metastasis.•FAO is reprogrammed in cancer and cancer-associated immune and other host cells.•FAO is druggable given the differential dependence of cancer and normal tissues.•FAO inhibitors including those for other ailments offer new anti-cancer therapies.
AbstractList	Cancer cells undergo metabolic reprogramming such as enhanced aerobic glycolysis, mutations in the tricarboxylic acid cycle enzymes, and upregulation of de novo lipid synthesis and glutaminolysis. These alterations are pivotal to the development and maintenance of the malignant phenotype of cancer cells in unfavorable tumor microenvironment or metastatic sites. Although mitochondrial fatty acid β-oxidation (FAO) is a primary bioenergetic source, it has not been generally recognized as part of the metabolic landscape of cancer. The last few years, however, have seen a dramatic change in the view of cancer relevance of the FAO pathway. Many recent studies have provided significant evidence to support a “lipolytic phenotype” of cancer. FAO, like other well-defined metabolic pathways involved in cancer, is dysregulated in diverse human malignancies. Cancer cells rely on FAO for proliferation, survival, stemness, drug resistance, and metastatic progression. FAO is also reprogrammed in cancer-associated immune and other host cells, which may contribute to immune suppression and tumor-promoting microenvironment. This article reviews and puts into context our current understanding of multi-faceted roles of FAO in oncogenesis as well as anti-cancer therapeutic opportunities posed by the FAO pathway. •FAO emerges as a new aspect of metabolic transformation in cancer.•Cancer cells rely on FAO for growth, stemness, drug resistance and metastasis.•FAO is reprogrammed in cancer and cancer-associated immune and other host cells.•FAO is druggable given the differential dependence of cancer and normal tissues.•FAO inhibitors including those for other ailments offer new anti-cancer therapies. Cancer cells undergo metabolic reprogramming such as enhanced aerobic glycolysis, mutations in the tricarboxylic acid cycle enzymes, and upregulation of de novo lipid synthesis and glutaminolysis. These alterations are pivotal to the development and maintenance of the malignant phenotype of cancer cells in unfavorable tumor microenvironment or metastatic sites. Although mitochondrial fatty acid β-oxidation (FAO) is a primary bioenergetic source, it has not been generally recognized as part of the metabolic landscape of cancer. The last few years, however, have seen a dramatic change in the view of cancer relevance of the FAO pathway. Many recent studies have provided significant evidence to support a “lipolytic phenotype” of cancer. FAO, like other well-defined metabolic pathways involved in cancer, is dysregulated in diverse human malignancies. Cancer cells rely on FAO for proliferation, survival, stemness, drug resistance, and metastatic progression. FAO is also reprogrammed in cancer-associated immune and other host cells, which may contribute to immune suppression and tumor-promoting microenvironment. This article reviews and puts into context our current understanding of multi-faceted roles of FAO in oncogenesis as well as anti-cancer therapeutic opportunities posed by the FAO pathway. Cancer cells undergo metabolic reprogramming such as enhanced aerobic glycolysis, mutations in the tricarboxylic acid cycle enzymes, and upregulation of de novo lipid synthesis and glutaminolysis. These alterations are pivotal to the development and maintenance of the malignant phenotype of cancer cells in unfavorable tumor microenvironment or metastatic sites. Although mitochondrial fatty acid β-oxidation (FAO) is a primary bioenergetic source, it has not been generally recognized as part of the metabolic landscape of cancer. The last few years, however, have seen a dramatic change in the view of cancer relevance of the FAO pathway. Many recent studies have provided significant evidence to support a "lipolytic phenotype" of cancer. FAO, like other well-defined metabolic pathways involved in cancer, is dysregulated in diverse human malignancies. Cancer cells rely on FAO for proliferation, survival, stemness, drug resistance, and metastatic progression. FAO is also reprogrammed in cancer-associated immune and other host cells, which may contribute to immune suppression and tumor-promoting microenvironment. This article reviews and puts into context our current understanding of multi-faceted roles of FAO in oncogenesis as well as anti-cancer therapeutic opportunities posed by the FAO pathway.Cancer cells undergo metabolic reprogramming such as enhanced aerobic glycolysis, mutations in the tricarboxylic acid cycle enzymes, and upregulation of de novo lipid synthesis and glutaminolysis. These alterations are pivotal to the development and maintenance of the malignant phenotype of cancer cells in unfavorable tumor microenvironment or metastatic sites. Although mitochondrial fatty acid β-oxidation (FAO) is a primary bioenergetic source, it has not been generally recognized as part of the metabolic landscape of cancer. The last few years, however, have seen a dramatic change in the view of cancer relevance of the FAO pathway. Many recent studies have provided significant evidence to support a "lipolytic phenotype" of cancer. FAO, like other well-defined metabolic pathways involved in cancer, is dysregulated in diverse human malignancies. Cancer cells rely on FAO for proliferation, survival, stemness, drug resistance, and metastatic progression. FAO is also reprogrammed in cancer-associated immune and other host cells, which may contribute to immune suppression and tumor-promoting microenvironment. This article reviews and puts into context our current understanding of multi-faceted roles of FAO in oncogenesis as well as anti-cancer therapeutic opportunities posed by the FAO pathway.
Author	Temkin, Sarah M. Wang, Xiang-Yang Ma, Yibao Wang, Wei Fang, Xianjun Hawkridge, Adam M. Guo, Chunqing
AuthorAffiliation	b Gynecologic Oncology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA c Department of Pharmaceutics, School of Pharmacy, Virginia Commonwealth University, Richmond, VA, 23298, USA a Department of Biochemistry & Molecular Biology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA d Human and Molecular Genetics, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA
AuthorAffiliation_xml	– name: b Gynecologic Oncology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA – name: c Department of Pharmaceutics, School of Pharmacy, Virginia Commonwealth University, Richmond, VA, 23298, USA – name: a Department of Biochemistry & Molecular Biology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA – name: d Human and Molecular Genetics, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA
Author_xml	– sequence: 1 givenname: Yibao orcidid: 0000-0002-3270-8893 surname: Ma fullname: Ma, Yibao organization: Department of Biochemistry & Molecular Biology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA – sequence: 2 givenname: Sarah M. surname: Temkin fullname: Temkin, Sarah M. organization: Gynecologic Oncology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA – sequence: 3 givenname: Adam M. surname: Hawkridge fullname: Hawkridge, Adam M. organization: Department of Pharmaceutics, School of Pharmacy, Virginia Commonwealth University, Richmond, VA, 23298, USA – sequence: 4 givenname: Chunqing surname: Guo fullname: Guo, Chunqing organization: Human and Molecular Genetics, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA – sequence: 5 givenname: Wei surname: Wang fullname: Wang, Wei organization: Department of Biochemistry & Molecular Biology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA – sequence: 6 givenname: Xiang-Yang surname: Wang fullname: Wang, Xiang-Yang organization: Human and Molecular Genetics, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA – sequence: 7 givenname: Xianjun surname: Fang fullname: Fang, Xianjun email: xianjun.fang@vcuhealth.org organization: Department of Biochemistry & Molecular Biology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/30102953$$D View this record in MEDLINE/PubMed
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SubjectTerms	Angina pectoris Apoptosis ATP Biosynthesis Breast cancer Cancer Cell growth Cell proliferation Cell Transformation, Neoplastic - metabolism Dehydrogenases Drug resistance Energy Metabolism Enzymes Fatty acid β-oxidation Fatty acids Fatty Acids - metabolism Genetic transformation Glycolysis Humans Kinases Leukemia Lipid Metabolism Lipolysis Lipolytic phenotype Medical research Medicine Metabolic pathways Metabolism Metastases Metastasis Mitochondria Mitochondria - metabolism NADPH Neoplasms - metabolism Neoplasms - pathology NMR Nuclear magnetic resonance Oxidation Oxidation-Reduction Phenotypes Prostate cancer Transgenic animals Tricarboxylic acid cycle Tumor Microenvironment Tumorigenesis
Title	Fatty acid oxidation: An emerging facet of metabolic transformation in cancer
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