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重塑脂质代谢以增强黑色素瘤免疫治疗效果:癌症治疗的前沿领域。

Rewiring lipid metabolism to enhance immunotherapy efficacy in melanoma: a frontier in cancer treatment.

作者信息

Xiong Lihua, Cheng Jian

机构信息

Department of Dermatology, Cheng Du Xinjin District Hospital of Traditional Chinese Medicine, Chengdu, China.

Department of Chinese Medicine, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.

出版信息

Front Oncol. 2025 May 1;15:1519592. doi: 10.3389/fonc.2025.1519592. eCollection 2025.


DOI:10.3389/fonc.2025.1519592
PMID:40376583
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12078133/
Abstract

Immunotherapy has transformed the landscape of melanoma treatment, offering significant extensions in survival for many patients. Despite these advancements, nearly 50% of melanoma cases remain resistant to such therapies, highlighting the need for novel approaches. Emerging research has identified lipid metabolism reprogramming as a key factor in promoting melanoma progression and resistance to immunotherapy. This reprogramming not only supports tumor growth and metastasis but also creates an immunosuppressive environment that impairs the effectiveness of treatments such as immune checkpoint inhibitors (ICIs). This review delves into the intricate relationship between lipid metabolism and immune system interactions in melanoma. We will explore how alterations in lipid metabolic pathways contribute to immune evasion and therapy resistance, emphasizing recent discoveries in this area. Additionally, we also highlights novel therapeutic strategies targeting lipid metabolism to enhance immune checkpoint inhibitor (ICI) efficacy.

摘要

免疫疗法已经改变了黑色素瘤的治疗格局,为许多患者带来了显著的生存期延长。尽管有这些进展,但仍有近50%的黑色素瘤病例对此类疗法耐药,这凸显了采用新方法的必要性。新兴研究已确定脂质代谢重编程是促进黑色素瘤进展和对免疫疗法耐药的关键因素。这种重编程不仅支持肿瘤生长和转移,还营造了一种免疫抑制环境,削弱了免疫检查点抑制剂(ICI)等治疗方法的有效性。本综述深入探讨黑色素瘤中脂质代谢与免疫系统相互作用之间的复杂关系。我们将探究脂质代谢途径的改变如何导致免疫逃逸和治疗耐药,重点介绍该领域的最新发现。此外,我们还强调了针对脂质代谢以提高免疫检查点抑制剂(ICI)疗效的新型治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0073/12078133/3974b02c7d14/fonc-15-1519592-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0073/12078133/3974b02c7d14/fonc-15-1519592-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0073/12078133/3974b02c7d14/fonc-15-1519592-g001.jpg

相似文献

[1]
Rewiring lipid metabolism to enhance immunotherapy efficacy in melanoma: a frontier in cancer treatment.

Front Oncol. 2025-5-1

[2]
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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
Secreted Apoe rewires melanoma cell state vulnerability to ferroptosis.

Sci Adv. 2024-10-18

[2]
TCTN1 Induces Fatty Acid Oxidation to Promote Melanoma Metastasis.

Cancer Res. 2025-1-2

[3]
The critical role of glutamine and fatty acids in the metabolic reprogramming of -resistant melanoma cells.

Front Pharmacol. 2024-8-8

[4]
Vitamin E and GPX4 cooperatively protect treg cells from ferroptosis and alleviate intestinal inflammatory damage in necrotizing enterocolitis.

Redox Biol. 2024-9

[5]
Cholesterol neutralized vemurafenib treatment by promoting melanoma stem-like cells via its metabolite 27-hydroxycholesterol.

Cell Mol Life Sci. 2024-5-22

[6]
Safety and biological outcomes following a phase 1 trial of GD2-specific CAR-T cells in patients with GD2-positive metastatic melanoma and other solid cancers.

J Immunother Cancer. 2024-5-15

[7]
Lipid metabolism in tumor-infiltrating regulatory T cells: perspective to precision immunotherapy.

Biomark Res. 2024-4-22

[8]
Cancer biomarkers: Emerging trends and clinical implications for personalized treatment.

Cell. 2024-3-28

[9]
Cystine deprivation triggers CD36-mediated ferroptosis and dysfunction of tumor infiltrating CD8 T cells.

Cell Death Dis. 2024-2-15

[10]
Tumor-secreted FGF21 acts as an immune suppressor by rewiring cholesterol metabolism of CD8T cells.

Cell Metab. 2024-3-5

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