Oxidative medicine and cellular longevity · 2026
The Lipid Line of Defence: Monounsaturated Fatty Acids (MUFAs) in Cancer and Ferroptosis.
СтатьяОбзорНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Baadkar Sneha D, Kandettu Amoolya, Ray Swagat, Chakrabarty Sanjiban
Аннотация
BACKGROUND: Monounsaturated 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.
AIM: This 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.
METHODS: Relevant experimental and clinical studies investigating MUFA metabolism, lipid metabolic reprogramming, ferroptosis and therapeutic interventions in cancer were comprehensively reviewed and critically analysed.
RESULTS: Enhanced 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.
CONCLUSION: MUFA 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.
AIM: This 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.
METHODS: Relevant experimental and clinical studies investigating MUFA metabolism, lipid metabolic reprogramming, ferroptosis and therapeutic interventions in cancer were comprehensively reviewed and critically analysed.
RESULTS: Enhanced 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.
CONCLUSION: MUFA 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.