肿瘤干细胞的多维分析：从生物学特性，代谢适应到免疫逃生机制

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，代谢适应和免疫逃生机制是当前肿瘤学研究的重点。 CSC具有自我更新，多方向分化和肿瘤性，并且可以通过克隆进化，分层模型和动态CSC模型来阐明其作用机制，因为该模型可以更好地识别其更好地识别CSC的功能和起源。 CSC的起源假设涉及细胞 - 细胞融合，水平基因转移，基因组不稳定性和微环境调节，它们共同塑造了CSC的多样性。在分类方面，CSC包括初级CSC（PRI-CSC），癌前的干细胞（PRE-CSC），迁移的CSC（MIG-CSC）和化学疗法耐药性CSCS（CR-CSC和RR-CSC），每种类型在肿瘤进展中都起着特定的作用。 CSC的表面标记，例如CD24，CD34，CD44，CD90，CD133，CD166，EPCAM和LGR5，提供了识别，隔离和靶向CSC的可能性，但其表达的不稳定性和异质性增加了治疗的困难。 CSC通过代谢重编程适应了它们的生存需求，表明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效应代表其代谢谱，改变谷氨酰胺和脂肪酸代谢进一步有助于CSC的快速增殖和存活。 CSC能够通过调节代谢网络以保持其干性特征，增强抗氧化剂防御并适应治疗应力来维持其干性。免疫逃生是CSC维持其生存的另一种策略，CSC可以通过上调PD-L1表达和促进免疫抑制微环境的形成，有效地逃避免疫监测。总之，这些特性揭示了CSC的多维复杂性，强调了对CSC生物学对开发更有效的肿瘤治疗策略的更深入了解的重要性。将来，针对CSC的疗法将集中在表面标记，代谢途径的干预以及克服免疫逃生的精确鉴定上，以改善癌症治疗的相关性和功效，并最终改善患者预后。

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.