ReviewOxidative medicine and cellular longevity2026
The Lipid Line of Defence: Monounsaturated Fatty Acids (MUFAs) in Cancer and Ferroptosis.
Review in Oxidative medicine and cellular longevity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
backgroundMonounsaturated fatty acid (MUFA) metabolism promotes cancer progression and survival by regulating membrane lipid composition, maintaining lipid homeostasis and preserving redox balance. A growing body of evidence indicates that altered MUFA metabolism promotes tumour growth while protecting cancer cells from ferroptosis.
aimThis review summarises current knowledge on the contributions of MUFA metabolism to carcinogenesis, regulation of ferroptosis and treatment response across different cancers. Further, we discussed the emerging treatment strategies targeting MUFA metabolic pathways.
methodsRelevant experimental and clinical studies investigating MUFA metabolism, lipid metabolic reprogramming, ferroptosis and therapeutic interventions in cancer were comprehensively reviewed and critically analysed.
resultsEnhanced de novo MUFA synthesis and incorporation into membrane phospholipids increase the MUFA-to-polyunsaturated fatty acid (PUFA) ratio, thereby reducing the availability of oxidation-prone PUFAs, limiting lipid peroxidation, and protecting cancer cells from ferroptosis. MUFA-driven membrane remodelling enhances membrane fluidity and activates oncogenic signalling pathways, including epithelial-mesenchymal transition (EMT), cancer cell migration, invasion and metastasis. These effects are mediated by the dysregulated expression of key lipogenic enzymes and signalling pathways that reprogramme lipid metabolism to meet the metabolic demands of cancer cells. Multiple studies have shown that MUFA metabolism is a promising therapeutic target. Furthermore, the inhibition of stearoyl-CoA desaturase-1 (SCD1) and fatty acid synthase (FASN), key enzymes in MUFA metabolism, sensitises cancer cells to ferroptosis by enhancing lipid peroxidation.
conclusionMUFA metabolism is a key regulator of cancer progression and ferroptosis resistance. Targeting MUFA metabolic pathways is a promising therapeutic strategy. However, mechanistic studies are required to elucidate the molecular mechanisms underlying sensitivity to ferroptosis and to optimise clinical applications.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.