Evidence map›Paper›PMID 40140862›Full record

ArticleLipids in health and disease2025

Arachidonic acid suppresses lung cancer cell growth and modulates lipid metabolism and the ERK/PPARγ signaling pathway.

Lin Wang, Lanlan Wei, Xueling Chen, Jiali Xiong

Abstract read
In one paragraph

Article in Lipids in health and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Pharmaceuticals (Basel, Switzerland) · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. Article
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

4 authors.

Lin WangDepartment of Respiratory and Critical Care Medicine, Zhuzhou Central Hospital, ZhuZhou, 412000, Hunan Province, China.
Lanlan WeiDepartment of Respiratory and Critical Care Medicine, Zhuzhou Central Hospital, ZhuZhou, 412000, Hunan Province, China.
Xueling ChenEmergency Center, Zhuzhou Central Hospital, ZhuZhou, 412000, Hunan Province, China.
Jiali XiongDepartment of Respiratory and Critical Care Medicine, Zhuzhou Central Hospital, ZhuZhou, 412000, Hunan Province, China. 18673371226@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer remains the leading cause of cancer-related mortality worldwide, necessitating the development of new treatment strategies. Arachidonic acid (ARA), a polyunsaturated fatty acid, shows promise in cancer therapy due to its potential anti-tumor effects, although its role in lung cancer remains unclear. This study investigated the effects and underlying mechanism of ARA on A549 and NCI-H1299 lung cancer cells. In vitro assays were used to assess cell viability, apoptosis, colony formation, lipid droplet formation, and changes in cellular lipid content. ARA dose-dependently suppressed cell viability, facilitated apoptosis, and suppressed colony formation in both lung cancer cell lines. Network pharmacology analysis was performed to identify potential gene targets and pathways, uncovering 61 overlapping genes between ARA and lung cancer-related targets, with mitogen-activated protein kinase 1 (MAPK1) emerging as a key gene. Enrichment analyses suggested that the effects of ARA might be mediated through lipid metabolism and the extracellular signal-regulated kinase (ERK)/peroxisome proliferator-activated receptor gamma (PPARγ) signaling pathway. In both lung cancer cell lines, ARA treatment inhibited lipid droplet formation and decreased the cellular lipids. Immunoblotting further confirmed that ARA treatment significantly increased ERK phosphorylation while reducing PPARγ and fatty acid synthase (FASN) protein levels. In vitro experiments using GW9662, a PPARγ antagonist, confirmed that inhibiting lipid droplet formation impairs lung cancer cell viability and promotes apoptosis. Furthermore, in vivo experiments demonstrated that ARA significantly reduced tumor size and weight in a lung cancer xenograft model, further validating its anti-tumor effects. The potential of ARA as a therapeutic agent for lung cancer might involve lipid metabolism and relevant signaling pathways. A future study exploring the full therapeutic potential of ARA and underlying mechanisms in lung cancer is needed.

Indexed as

Arachidonic AcidLipid MetabolismLung NeoplasmsPPAR gammaA549 CellsAnilidesAnimalsApoptosisCell Line, TumorCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticHumansMAP Kinase Signaling SystemMiceSignal TransductionAnilidesArachidonic AcidPPAR gammaPPARG protein, humanArachidonic acid (ARA)Lipid metabolismLung cancerMitogen-activated protein kinase 1 (MAPK1)The extracellular signal-regulated kinase (ERK)/peroxisome proliferator-activated receptor gamma (PPARγ) pathway

Identifiers

PMID40140862
PMCPMC11948643

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.