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Cancer Lett. 2018 Oct 28;435:92-100. doi: 10.1016/j.canlet.2018.08.006. Epub 2018 Aug 10.

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

Author information

1
Department of Biochemistry & Molecular Biology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA.
2
Gynecologic Oncology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA.
3
Department of Pharmaceutics, School of Pharmacy, Virginia Commonwealth University, Richmond, VA, 23298, USA.
4
Human and Molecular Genetics, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA.
5
Department of Biochemistry & Molecular Biology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA. Electronic address: xianjun.fang@vcuhealth.org.

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.

KEYWORDS:

ATP; Cancer; Fatty acid β-oxidation; Lipolytic phenotype; NADPH

PMID:
30102953
PMCID:
PMC6240910
[Available on 2019-10-28]
DOI:
10.1016/j.canlet.2018.08.006

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