{"title":"Emerging roles of small extracellular vesicles in metabolic reprogramming and drug resistance in cancers.","authors":"Jingcun Shi, Ying Shen, Jianjun Zhang","doi":"10.20517/cdr.2024.81","DOIUrl":null,"url":null,"abstract":"<p><p>Studies of carcinogenic metabolism have shown that cancer cells have significant metabolic adaptability and that their metabolic dynamics undergo extensive reprogramming, which is a fundamental feature of cancer. The Warburg effect describes the preference of cancer cells for glycolysis over oxidative phosphorylation (OXPHOS), even under aerobic conditions. However, metabolic reprogramming in cancer cells involves not only glycolysis but also changes in lipid and amino acid metabolism. The mechanisms of these metabolic shifts are critical for the discovery of novel cancer therapeutic targets. Despite advances in the field of oncology, chemotherapy resistance, including multidrug resistance, remains a challenge. Research has revealed a correlation between metabolic reprogramming and anticancer drug resistance, but the underlying complex mechanisms are not fully understood. In addition, small extracellular vesicles (sEVs) may play a role in expanding metabolic reprogramming and promoting the development of drug resistance by mediating intercellular communication. The aim of this review is to assess the metabolic reprogramming processes that intersect with resistance to anticancer therapy, with particular attention given to the changes in glycolysis, lipid metabolism, and amino acid metabolism that accompany this phenomenon. In addition, the role of sEVs in disseminating metabolic reprogramming and promoting the development of drug-resistant phenotypes will be critically evaluated.</p>","PeriodicalId":70759,"journal":{"name":"癌症耐药(英文)","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11472704/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"癌症耐药(英文)","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.20517/cdr.2024.81","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Studies of carcinogenic metabolism have shown that cancer cells have significant metabolic adaptability and that their metabolic dynamics undergo extensive reprogramming, which is a fundamental feature of cancer. The Warburg effect describes the preference of cancer cells for glycolysis over oxidative phosphorylation (OXPHOS), even under aerobic conditions. However, metabolic reprogramming in cancer cells involves not only glycolysis but also changes in lipid and amino acid metabolism. The mechanisms of these metabolic shifts are critical for the discovery of novel cancer therapeutic targets. Despite advances in the field of oncology, chemotherapy resistance, including multidrug resistance, remains a challenge. Research has revealed a correlation between metabolic reprogramming and anticancer drug resistance, but the underlying complex mechanisms are not fully understood. In addition, small extracellular vesicles (sEVs) may play a role in expanding metabolic reprogramming and promoting the development of drug resistance by mediating intercellular communication. The aim of this review is to assess the metabolic reprogramming processes that intersect with resistance to anticancer therapy, with particular attention given to the changes in glycolysis, lipid metabolism, and amino acid metabolism that accompany this phenomenon. In addition, the role of sEVs in disseminating metabolic reprogramming and promoting the development of drug-resistant phenotypes will be critically evaluated.
对致癌新陈代谢的研究表明,癌细胞具有很强的新陈代谢适应能力,其新陈代谢动态会发生广泛的重编程,这是癌症的一个基本特征。沃伯格效应描述了癌细胞对糖酵解的偏好,而不是氧化磷酸化(OXPHOS),即使在有氧条件下也是如此。然而,癌细胞的代谢重编程不仅涉及糖酵解,还包括脂质和氨基酸代谢的变化。这些代谢转变的机制对于发现新型癌症治疗靶点至关重要。尽管肿瘤学领域取得了进展,但化疗耐药性(包括多药耐药性)仍是一项挑战。研究发现,代谢重编程与抗癌药物耐药性之间存在相关性,但其背后的复杂机制尚未完全明了。此外,细胞外小泡(sEVs)可能通过介导细胞间通讯,在扩大代谢重编程和促进耐药性发展方面发挥作用。本综述旨在评估与抗癌治疗耐药性交织在一起的代谢重编程过程,尤其关注伴随这一现象出现的糖酵解、脂质代谢和氨基酸代谢的变化。此外,还将严格评估 sEV 在传播代谢重编程和促进耐药表型发展方面的作用。