Evidence map›Paper›PMID 30008815›Full record

ReviewOncology letters2018

Fatty acid activation in carcinogenesis and cancer development: Essential roles of long-chain acyl-CoA synthetases.

Yue Tang, Jing Zhou, Shing Chuan Hooi, Yue-Ming Jiang, Guo-Dong Lu

Open access · diamondAbstract readReview
In one paragraph

Review in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

125 citing papers in PubMed, 153 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. The Association ofBalkan journal of medical genetics : BJMG · 2025
    Article
  10. Article
  11. Metabolic Regulation of Ferroptosis in Breast Cancer.International journal of molecular sciences · 2025
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Ferroptosis: CD8Cell death discovery · 2025
    Review

65 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

5 authors at 2 institutions in 2 countries.

Yue TangDepartment of Toxicology, School of Public Health, Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Jing ZhouDepartment of Physiology, School of Preclinical Medicine, Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Shing Chuan HooiDepartment of Physiology, Yong Loo Lim School of Medicine, National University of Singapore, Singapore 117543, Republic of Singapore.
Yue-Ming JiangDepartment of Toxicology, School of Public Health, Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Guo-Dong LuDepartment of Toxicology, School of Public Health, Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Guangxi Medical University · CNNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The significance of fatty acid metabolism in cancer initiation and development is increasingly accepted by scientists and the public due to the high prevalence of overweight and obese individuals. Fatty acids have different turnovers in the body: Either breakdown into acetyl-CoA to aid ATP generation through catabolic metabolism or incorporation into triacylglycerol and phospholipid through anabolic metabolism. However, these two distinct pathways require a common initial step known as fatty acid activation. Long-chain acyl-CoA synthetases (ACSLs), which are responsible for activation of the most abundant long-chain fatty acids, are commonly deregulated in cancer. This deregulation is also associated with poor survival in patients with cancer. Fatty acids physiologically regulate ACSL expression, but cancer cells could hijack certain involved regulatory mechanisms to deregulate ACSLs. Among the five family isoforms, ACSL1 and ACSL4 are able to promote ungoverned cell growth, facilitate tumor invasion and evade programmed cell death, while ACSL3 may have relatively complex functions in different types of cancer. Notably, ACSL4 is also essential for the induction of ferroptosis (another form of programmed cell death) by facilitating arachidonic acid oxidation, which makes the enzyme a desirable cancer target. The present review thus evaluates the functions of deregulated ACSLs in cancer, the possible molecular mechanisms involved and the chemotherapeutic potentials to target ACSLs. A better understanding of the pathological effects of ACSLs in cancer and the involved molecular mechanisms will aid in delineating the exact role of fatty acid metabolism in cancer and designing precise cancer prevention and treatment strategies.

Indexed as

cancer developmentcarcinogenesiscell deathfatty acidslong-chain acyl-CoA synthetasesmetabolism

Identifiers

PMID30008815
PMCPMC6036470
OpenAlexW2807141660

What OpenQuestion holds

Textmetadata
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.