Evidence map›Paper›PMID 30102953›Full record

ReviewCancer letters2018

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

Yibao Ma, Sarah M Temkin, Adam M Hawkridge, Chunqing Guo, Wei Wang, Xiang-Yang Wang, Xianjun Fang

Abstract readReview
In one paragraph

Review in Cancer letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 339 papers.

0numbers the graph read from it
0cells of the map it votes in
339citing 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

339 citing papers in PubMed.

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279 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.

Yibao MaDepartment of Biochemistry & Molecular Biology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA.
Sarah M TemkinGynecologic Oncology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA.
Adam M HawkridgeDepartment of Pharmaceutics, School of Pharmacy, Virginia Commonwealth University, Richmond, VA, 23298, USA.
Chunqing GuoHuman and Molecular Genetics, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA.
Wei WangDepartment of Biochemistry & Molecular Biology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA.
Xiang-Yang WangHuman and Molecular Genetics, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA.
Xianjun FangDepartment of Biochemistry & Molecular Biology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298, USA. Electronic address: xianjun.fang@vcuhealth.org.

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Keri R Maher · 1985 to 2026
$51.0M
Large heat shock proteins and their role in cancer therapyR01CA099326 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI REPASKY, ELIZABETH A, WANG, XIANG-YANG SHAWN · 2003 to 2020
$5.7M
Host-tumor interactions and cancer relapse after radiation therapyR01CA175033 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI WANG, XIANG-YANG SHAWN · 2014 to 2018
$1.6M
NCI NIH HHS P30 CA016059NCI NIH HHS R01 CA099326NCI NIH HHS R01 CA175033
6 · The paper itself

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.

Indexed as

Energy MetabolismCell Transformation, NeoplasticFatty AcidsHumansLipid MetabolismLipolysisMitochondriaNeoplasmsOxidation-ReductionTumor MicroenvironmentFatty AcidsATPCancerFatty acid β-oxidationLipolytic phenotypeNADPH

Identifiers

PMID30102953
PMCPMC6240910

What OpenQuestion holds

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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.