作为肿瘤发生、进展、复发和转移的关键因素，CSC的生物学特性、代谢适应和免疫逃逸机制是当前肿瘤学研究的重点。 CSCs具有自我更新、多向分化和致瘤性，其作用机制可以通过克隆进化、层次模型和动态CSCs模型来阐明，其中动态模型因其更好地解释功能和起源而受到广泛认可CSC 的数量。 CSCs的起源假说涉及细胞间融合、水平基因转移、基因组不稳定性和微环境调节，这些共同塑造了CSCs的多样性。从分类上看，CSCs包括原发性CSCs（pri-CSCs）、癌前干细胞（pre-CSCs）、迁移性CSCs（mig-CSCs）和化疗耐药CSCs（cr-CSCs和rr-CSCs）。每种类型在肿瘤进展中都发挥着特定的作用。 CSCs的表面标志物，如CD24、CD34、CD44、CD90、CD133、CD166、EpCAM和LGR5等，为识别、分离和靶向CSCs提供了可能性，但其表达的不稳定性和异质性增加了治疗难度。 CSC 通过代谢重编程来适应其生存需求，表现出在糖酵解和氧化磷酸化 (OXPHOS) 之间灵活切换的能力，以及对氨基酸和脂质代谢的调整。 Warburg 效应代表了它们的代谢特征，而谷氨酰胺和脂肪酸代谢的改变进一步促进了 CSC 的快速增殖和存活。 CSC能够通过调节代谢网络来维持其干性特征、增强抗氧化防御并适应治疗应激。免疫逃逸是CSC维持生存的另一种策略，CSC可以通过上调PD-L1表达、促进免疫抑制微环境形成等机制有效逃避免疫监视。这些特性共同揭示了 CSC 的多维复杂性，强调了深入了解 CSC 生物学对于开发更有效的肿瘤治疗策略的重要性。未来，针对CSC的治疗将侧重于表面标志物的精确识别、代谢途径的干预以及克服免疫逃逸，以提高癌症治疗的相关性和疗效，最终改善患者的预后。Copyright © 2024 Han,何、吴、何、周。

As a key factor in tumorigenesis, progression, recurrence and metastasis, the biological properties, metabolic adaptations and immune escape mechanisms of CSCs are the focus of current oncological research. CSCs possess self-renewal, multidirectional differentiation and tumorigenicity, and their mechanisms of action can be elucidated by the clonal evolution, hierarchical model and the dynamic CSCs model, of which the dynamic model is widely recognized due to its better explanation of the function and origin of CSCs. The origin hypothesis of CSCs involves cell-cell fusion, horizontal gene transfer, genomic instability and microenvironmental regulation, which together shape the diversity of CSCs. In terms of classification, CSCs include primary CSCs (pri-CSCs), precancerous stem cells (pre-CSCs), migratory CSCs (mig-CSCs), and chemo-radiotherapy-resistant CSCs (cr-CSCs and rr-CSCs), with each type playing a specific role in tumor progression. Surface markers of CSCs, such as CD24, CD34, CD44, CD90, CD133, CD166, EpCAM, and LGR5, offer the possibility of identifying, isolating, and targeting CSCs, but the instability and heterogeneity of their expression increase the difficulty of treatment. CSCs have adapted to their survival needs through metabolic reprogramming, showing the ability to flexibly switch between glycolysis and oxidative phosphorylation (OXPHOS), as well as adjustments to amino acid and lipid metabolism. The Warburg effect typifies their metabolic profiles, and altered glutamine and fatty acid metabolism further contributes to the rapid proliferation and survival of CSCs. CSCs are able to maintain their stemness by regulating the metabolic networks to maintain their stemness characteristics, enhance antioxidant defences, and adapt to therapeutic stress. Immune escape is another strategy for CSCs to maintain their survival, and CSCs can effectively evade immune surveillance through mechanisms such as up-regulating PD-L1 expression and promoting the formation of an immunosuppressive microenvironment. Together, these properties reveal the multidimensional complexity of CSCs, underscoring the importance of a deeper understanding of the biology of CSCs for the development of more effective tumor therapeutic strategies. In the future, therapies targeting CSCs will focus on precise identification of surface markers, intervention of metabolic pathways, and overcoming immune escape, with the aim of improving the relevance and efficacy of cancer treatments, and ultimately improving patient prognosis.Copyright © 2024 Han, He, Wu, He and Zhou.