Metabolic reprogramming provides tumors with an energy source and biofuel to support their survival in the malignant microenvironment. Extensive research into the intrinsic oncogenic mechanisms of the tumor microenvironment (TME) has established that cancer-associated fibroblast (CAFs) and metabolic reprogramming regulates tumor progression through numerous biological activities, including tumor immunosuppression, chronic inflammation, and ecological niche remodeling. Specifically, immunosuppressive TME formation is promoted and mediators released via CAFs and multiple immune cells that collectively support chronic inflammation, thereby inducing pre-metastatic ecological niche formation, and ultimately driving a vicious cycle of tumor proliferation and metastasis. This review comprehensively explores the process of CAFs and metabolic regulation of the dynamic evolution of tumor-adapted TME, with particular focus on the mechanisms by which CAFs promote the formation of an immunosuppressive microenvironment and support metastasis. Existing findings confirm that multiple components of the TME act cooperatively to accelerate the progression of tumor events. The potential applications and challenges of targeted therapies based on CAFs in the clinical setting are further discussed in the context of advancing research related to CAFs.

中文翻译：

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癌症相关成纤维细胞和代谢重编程：揭示肿瘤进化中错综复杂的串扰


代谢重编程为肿瘤提供能源和生物燃料，以支持它们在恶性微环境中的生存。对肿瘤微环境（TME）内在致癌机制的广泛研究表明，癌症相关成纤维细胞（CAF）和代谢重编程通过多种生物活性调节肿瘤进展，包括肿瘤免疫抑制、慢性炎症和生态位重塑。具体而言，通过CAF和多种免疫细胞促进免疫抑制性TME形成并释放介质，共同支持慢性炎症，从而诱导转移前生态位形成，最终驱动肿瘤增殖和转移的恶性循环。本文全面探讨了CAFs的过程和肿瘤适应TME动态进化的代谢调节，特别关注CAFs促进免疫抑制微环境形成和支持转移的机制。现有研究结果证实，TME 的多个成分协同作用，加速肿瘤事件的进展。在推进 CAF 相关研究的背景下，进一步讨论了基于 CAF 的靶向治疗在临床环境中的潜在应用和挑战。