Chen Haoran, Fang Suping, Zhu Xudong, Liu Hao
Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Front Cell Dev Biol. 2024 Jul 18;12:1412337. doi: 10.3389/fcell.2024.1412337. eCollection 2024.
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.
前列腺癌干细胞（PCSCs）是前列腺癌发展和治疗耐药性的主要驱动因素，其功能异质性和生态位已引起了相当多的研究关注。癌症相关成纤维细胞（CAFs）是肿瘤微环境（TME）的关键组成部分，会显著影响PCSC的干性。此外，CAFs通过释放信号分子和改变周围环境来促进PCSC的生长和存活。相反，PCSCs可能通过产生各种分子来影响CAFs的特征和行为。这种相互作用机制可能对前列腺癌的进展和治疗耐药性的产生至关重要。利用类器官对TME进行建模能够深入研究CAF-PCSC相互作用，为准确评估潜在靶基因和设计前列腺癌新治疗策略提供了有价值的临床前工具。本综述的目的是讨论目前关于CAF-PCSC相互作用和串扰背后的多层次多靶点调控机制的研究，旨在为应对前列腺癌治疗挑战的治疗方法提供信息。
