Programa de Maestría y Doctorado en Ciencias Biológicas, Facultad de Ciencias, Universidad Nacional Autónoma de México, México City, México.
Laboratory of Virus and Cancer, Unidad de Investigacion Biomedica en Cáncer, Instituto de Investigaciones Biomedicas, Universidad Nacional Autonoma de Mexico & Subdireccion de Investigacion Basica, Instituto Nacional de Cancerologia, Secretaria de Salud, Ciudad de Mexico, Mexico.
Curr Stem Cell Res Ther. 2019;14(5):405-420. doi: 10.2174/1574888X13666180821154752.
Cancer Stem Cells (CSC) generally constitute a minor cellular population within tumors that exhibits some capacities of normal Stem Cells (SC). The existence of CSC, able to self-renew and differentiate, influences central aspects of tumor biology, in part because they can continue tumor growth, give rise to metastasis, and acquire drug and radioresistance, which open new avenues for therapeutics. It is well known that SC constantly interacts with their niche, which includes mesenchymal cells, extracellular ligands, and the Extra Cellular Matrix (ECM). These interactions regularly lead to homeostasis and maintenance of SC characteristics. However, the exact participation of each of these components for CSC maintenance is not clear, as they appear to be context- or cell-specific. In the recent past, surface cellular markers have been fundamental molecular tools for identifying CSC and distinguishing them from other tumor cells. Importantly, some of these cellular markers have been shown to possess functional roles that affect central aspects of CSC. Likewise, some of these markers can participate in regulating the interaction of CSC with their niche, particularly the ECM. We focused this review on the molecular mechanisms of surface cellular markers commonly employed to identify CSC, highlighting the signaling pathways and mechanisms involved in CSC-ECM interactions, through each of the cellular markers commonly used in the study of CSC, such as CD44, CD133, CD49f, CD24, CXCR4, and LGR5. Their presence does not necessarily implicate them in CSC biology.
癌症干细胞（CSC）通常构成肿瘤中一小部分具有某些正常干细胞（SC）特性的细胞。CSC 的存在，能够自我更新和分化，影响肿瘤生物学的核心方面，部分原因是它们可以继续肿瘤生长、引发转移，并获得药物和放射抗性，这为治疗开辟了新途径。众所周知，SC 不断与其龛位相互作用，龛位包括间充质细胞、细胞外配体和细胞外基质（ECM）。这些相互作用通常导致 SC 特性的平衡和维持。然而，对于 CSC 维持而言，这些成分中的每一个的确切参与并不清楚，因为它们似乎是特定于环境或特定于细胞的。在最近的过去，表面细胞标记物一直是鉴定 CSC 并将其与其他肿瘤细胞区分开来的重要分子工具。重要的是，其中一些细胞标记物已被证明具有影响 CSC 核心方面的功能作用。同样，这些标记物中的一些可以参与调节 CSC 与其龛位的相互作用，特别是与 ECM 的相互作用。我们专注于用于鉴定 CSC 的常见表面细胞标记物的分子机制，强调涉及 CSC-ECM 相互作用的信号通路和机制，通过常用于 CSC 研究的每个细胞标记物，如 CD44、CD133、CD49f、CD24、CXCR4 和 LGR5。它们的存在并不一定意味着它们与 CSC 生物学有关。
