癌症干细胞（CSC）具有高度致瘤性、化学抗性和免疫逃避性。它们成为产生大量肿瘤块、改变肿瘤微环境（TME）并利用它的核心驱动因素，导致癌症患者的临床结果不佳。因此，CSC 的存在是传统疗法和免疫监视失败的原因。识别实体瘤中的 CSC 仍然是现代肿瘤学中的一个重大挑战，使用细胞表面标记物是研究、分离和富集这些细胞的主要策略。在这篇综述中，我们探索了 CSC 标记，重点关注驱动 CSC 自我更新的潜在信号通路，这同时使它们具有内在的化学抗性和免疫系统逃避能力。我们全面讨论 CSC 的自主和非自主功能，特别强调它们与肿瘤微环境，特别是免疫细胞的相互作用。这种互惠网络增强了 CSC 的恶性程度，同时损害了周围的生态位，最终确定了与每个 CSC 标志物相关的治疗脆弱性。本次综述中提到的最常见的 CSC 表面标志物——CD44、CD133、ICAM1/CD54 和 LGR5——提供了对化疗耐药性和免疫逃避这两种疾病根除中至关重要的现象之间相互作用的见解。这种对最先进 CSC 的新视角无疑将为治疗开辟新途径。版权所有 © 2024。由 Elsevier Inc. 出版。

Cancer Stem Cells (CSCs) are highly tumorigenic, chemoresistant, and immune evasive. They emerge as a central driver that gives rise to the bulk of tumoral mass, modifies the tumor microenvironment (TME), and exploits it, leading to poor clinical outcomes for patients with cancer. The existence of CSCs thus accounts for the failure of conventional therapies and immune surveillance. Identifying CSCs in solid tumors remains a significant challenge in modern oncology, with the use of cell surface markers being the primary strategy for studying, isolating, and enriching these cells. In this review, we explore CSC markers, focusing on the underlying signaling pathways that drive CSC self-renewal, which simultaneously makes them intrinsically chemoresistant and immune system evaders. We comprehensively discuss the autonomous and non-autonomous functions of CSCs, with particular emphasis on their interactions with the tumor microenvironment, especially immune cells. This reciprocal network enhances CSCs malignancy while compromising the surrounding niche, ultimately defining therapeutic vulnerabilities associated with each CSC marker. The most common CSCs surface markers addressed in this review-CD44, CD133, ICAM1/CD54, and LGR5-provide insights into the interplay between chemoresistance and immune evasion, two critically important phenomena in disease eradication. This new perspective on the state-of-the-art of CSCs will undoubtedly open new avenues for therapy.Copyright © 2024. Published by Elsevier Inc.