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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 classi fi cation, 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 speci fi c 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 dif fi culty of treatment.CSCs have adapted to their survival needs through metabolic reprogramming, showing the ability to fl exibly switch between glycolysis and oxidative phosphorylation (OXPHOS), as well as adjustments to amino acid and lipid metabolism.The Warburg effect typi fi es their metabolic pro fi les, and altered glutamine and fatty acid metabolism further contributes to the rapid proliferation and survival of CSCs.CSC能够通过调节代谢网络来保持其干性特征，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可以通过诸如调节PD-L1表达的机制有效地逃避免疫监视，并促进免疫抑制性微环境的形成。一起，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肿瘤治疗策略的发展的重要性。将来，针对CSC的疗法将集中于表面标记物的精确鉴定，代谢途径的干预以及克服免疫逃生，以改善癌症治疗的相关性和效率，并最终改善患者的预后。
肿瘤干细胞的多维分析
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