Abstract:
The functional heterogeneity and ecological niche of prostate cancer stem cells (PCSCs), which are major drivers of prostate cancer development and treatment resistance, have attracted considerable research attention. Cancer-associated fibroblasts (CAFs), which are crucial components of the tumor microenvironment (TME), substantially affect PCSC stemness. Additionally, CAFs promote PCSC growth and survival by releasing signaling molecules and modifying the surrounding environment. Conversely, PCSCs may affect the characteristics and behavior of CAFs by producing various molecules. This crosstalk mechanism is potentially crucial for prostate cancer progression and the development of treatment resistance. Using organoids to model the TME enables an in-depth study of CAF-PCSC interactions, providing a valuable preclinical tool to accurately evaluate potential target genes and design novel treatment strategies for prostate cancer. The objective of this review is to discuss the current research on the multilevel and multitarget regulatory mechanisms underlying CAF-PCSC interactions and crosstalk, aiming to inform therapeutic approaches that address challenges in prostate cancer treatment.
摘要:
前列腺癌干细胞的功能异质性和生态位,它们是前列腺癌发展和治疗抵抗的主要驱动因素,已经引起了相当多的研究关注。癌症相关成纤维细胞(CAFs),它们是肿瘤微环境(TME)的关键组成部分,大大影响PCSC的干性。此外,CAF通过释放信号分子和改变周围环境来促进PCSC生长和存活。相反,PCSCs可能通过产生各种分子来影响CAFs的特性和行为。这种串扰机制对于前列腺癌的进展和治疗抗性的发展可能至关重要。使用类器官对TME进行建模,可以深入研究CAF-PCSC相互作用,提供了一个有价值的临床前工具来准确评估潜在的靶基因和设计新的前列腺癌治疗策略。这篇综述的目的是讨论当前关于CAF-PCSC相互作用和串扰的多水平和多目标调节机制的研究,旨在为解决前列腺癌治疗挑战的治疗方法提供信息。