Abstract：
Cancer-associated fibroblasts (CAFs) are crucial component of tumor microenvironment (TME) which undergo significant phenotypic changes and metabolic reprogramming, profoundly impacting tumor growth. This review delves into CAF plasticity, diverse origins, and the molecular mechanisms driving their continuous activation. Emphasis is placed on the intricate bidirectional crosstalk between CAFs and tumor cells, promoting cancer cell survival, proliferation, invasion, and immune evasion. Metabolic reprogramming, a cancer hallmark, extends beyond cancer cells to CAFs, contributing to the complex metabolic interplay within the TME. The \'reverse Warburg effect\' in CAFs mirrors the Warburg effect, involving the export of high-energy substrates to fuel cancer cells, supporting their rapid proliferation. Molecular regulations by key players like p53, Myc, and K-RAS orchestrate this metabolic adaptation. Understanding the metabolic symbiosis between CAFs and tumor cells opens avenues for targeted therapeutic strategies to disrupt this dynamic crosstalk. Unraveling CAF-mediated metabolic reprogramming provides valuable insights for developing novel anticancer therapies. This comprehensive review consolidates current knowledge, shedding light on CAFs\' multifaceted roles in the TME and offering potential targets for future therapies.
摘要：
肿瘤相关成纤维细胞（CAFs）是肿瘤微环境（TME）的重要组成部分，它经历了显著的表型变化和代谢重编程，深刻影响肿瘤生长。这篇综述深入研究了CAF可塑性，不同的起源,以及驱动它们持续激活的分子机制。重点放在CAFs和肿瘤细胞之间复杂的双向串扰，促进癌细胞存活，扩散,入侵,和免疫逃避。代谢重编程，癌症的标志，从癌细胞延伸到CAFs，有助于TME内复杂的代谢相互作用。CAF中的“反向Warburg效果”反映了Warburg效果，涉及向癌细胞输出高能底物，支持他们的迅速扩散。像p53，Myc，和K-RAS协调这种代谢适应。了解CAF和肿瘤细胞之间的代谢共生为靶向治疗策略打破这种动态串扰开辟了途径。解开CAF介导的代谢重编程为开发新的抗癌疗法提供了有价值的见解。这项全面的审查巩固了当前的知识，阐明CAFs在TME中的多方面作用，并为未来的治疗提供潜在的靶点。
