脂质代谢
重编程
转移
肿瘤微环境
癌症研究
肿瘤进展
生物
肝细胞癌
癌症
脂滴
生物信息学
细胞生物学
细胞
肿瘤细胞
生物化学
遗传学
作者
Mengke Wang,Houshan Lyu,Yuxin Liu,Yang Sun
标识
DOI:10.2174/0115680266366687250730060318
摘要
Abstract: Hepatocellular Carcinoma (HCC) represents a common malignant tumor worldwide, having a profound effect on human health. The processes of invasion and spreading to distant sites are critical malignant biological behaviors exhibited by tumors. The metabolic environment is intricately linked to the initiation, invasion, and subsequent dissemination of tumor cells, with a particular emphasis on lipid metabolism. Lipid metabolism plays a vital role in mediating membrane structure, providing energy, and facilitating signal transduction. It not only delivers energy sources for tumor cells but also establishes conditions conducive to the initiation, progression, and spread of HCC. To meet their energy demands, tumor cells undergo a process of lipid metabolic reprogramming, characterized here as abnormal lipid metabolism. Therefore, a comprehensive investigation into the mechanisms underpinning lipid metabolic reprogramming and its influence on HCC growth and dissemination is crucial for the prevention, early detection, and identification of novel therapeutic targets for HCC. This article initially delineates the metabolic pathways of fatty acids within cells during the development and progression of HCC. It then reviews recent advancements in understanding abnormal lipid metabolism, focusing on the associated genes, enzymes, proteins, and metabolic products that promote HCC progression and spread. Furthermore, a brief overview of the Tumor Immune Microenvironment (TIME) in HCC is provided, highlighting the interactions between Tumor-Associated Macrophages (TAMs) and HCC lipid metabolic reprogramming, as well as their effects on HCC growth and dissemination. Lastly, it examines the treatments targeting abnormal lipid metabolism in HCC utilizing Traditional Chinese Medicine (TCM) and natural products, offering new perspectives for targeting HCC lipid metabolic reprogramming to inhibit spread and invasion.
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