肿瘤-脂肪组织串联过程中的细胞外囊泡:癌症恶病质的关键驱动因素和治疗靶点

Cátia C Ramos, José Pires, Esperanza González, C. Garcia-Vallicrosa, Celso A. Reis, J. Falcón-Perez, D. Freitas
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引用次数: 0

摘要

癌症恶病质是一种复杂的代谢综合征,其特点是骨骼肌和身体脂肪的无意损失。这种综合征经常与不同类型的癌症有关,并对这些患者的预后和疗效产生负面影响。它涉及肿瘤细胞和脂肪组织之间的动态相互作用,其中肿瘤衍生的细胞外囊泡 (EVs) 在介导细胞间交流方面发挥着至关重要的作用。肿瘤细胞释放的细胞外囊泡含有生物活性分子,如激素(肾上腺髓质素、PTHrP)、促炎细胞因子(IL-6)和 miRNA(miR-1304-3p、miR-204-5p、miR-155、miR-425-3p、miR-146b-5p、miR-92a-3p),这些分子可引发脂肪分解,诱导白色脂肪细胞褐变,从而形成癌症恶病质表型。另一方面,脂肪细胞衍生的 EVs 可通过运输脂肪酸和参与脂肪酸氧化的酶来重编程肿瘤细胞的新陈代谢,从而导致肿瘤的生长和进展。这些囊泡还携带瘦素和关键的 miRNA(miR-155-5p、miR-10a-3p、miR-30a-3p、miR-32a/b、miR-21),从而支持肿瘤细胞的增殖、转移和耐药性。了解肿瘤细胞和脂肪细胞之间由 EV 介导的错综复杂的交流网络,能为了解癌症恶病质的驱动机制提供重要见解。这篇综述整合了目前关于由 EVs 介导的肿瘤细胞与脂肪组织之间串联的知识,并为未来研究提供了宝贵的见解。它还探讨了该领域存在争议的话题,以及控制癌症恶病质并最终改善患者预后和生活质量的可能治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Extracellular vesicles in tumor-adipose tissue crosstalk: key drivers and therapeutic targets in cancer cachexia
Cancer cachexia is a complex metabolic syndrome characterized by unintentional loss of skeletal muscle and body fat. This syndrome is frequently associated with different types of cancer and negatively affects the prognosis and outcome of these patients. It involves a dynamic interplay between tumor cells and adipose tissue, where tumor-derived extracellular vesicles (EVs) play a crucial role in mediating intercellular communication. Tumor cells release EVs containing bioactive molecules such as hormones (adrenomedullin, PTHrP), pro-inflammatory cytokines (IL-6), and miRNAs (miR-1304-3p, miR-204-5p, miR-155, miR-425-3p, miR-146b-5p, miR-92a-3p), which can trigger lipolysis and induce the browning of white adipocytes contributing to a cancer cachexia phenotype. On the other hand, adipocyte-derived EVs can reprogram the metabolism of tumor cells by transporting fatty acids and enzymes involved in fatty acid oxidation, resulting in tumor growth and progression. These vesicles also carry leptin and key miRNAs (miR-155-5p, miR-10a-3p, miR-30a-3p, miR-32a/b, miR-21), thereby supporting tumor cell proliferation, metastasis formation, and therapy resistance. Understanding the intricate network underlying EV-mediated communication between tumor cells and adipocytes can provide critical insights into the mechanisms driving cancer cachexia. This review consolidates current knowledge on the crosstalk between tumor cells and adipose tissue mediated by EVs and offers valuable insights for future research. It also addresses controversial topics in the field and possible therapeutic approaches to manage cancer cachexia and ultimately improve patient outcomes and quality of life.
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