In the realm of cancer research, the tumor microenvironment (TME) plays a crucial role in tumor initiation and progression, shaped by complex interactions between cancer cells and surrounding non-cancerous cells. Cytokines, as essential immunomodulatory agents, are secreted by various cellular constituents within the TME, including immune cells, cancer-associated fibroblasts, and cancer cells themselves. These cytokines facilitate intricate communication networks that significantly influence tumor initiation, progression, metastasis, and immune suppression. Pyroptosis contributes to TME remodeling by promoting the release of pro-inflammatory cytokines and sustaining chronic inflammation, impacting processes such as immune escape and angiogenesis. However, challenges remain due to the complex interplay among cytokines, pyroptosis, and the TME, along with the dual effects of pyroptosis on cancer progression and therapy-related complications like cytokine release syndrome. Unraveling these complexities could facilitate strategies that balance inflammatory responses while minimizing tissue damage during therapy. This review delves into the complex crosstalk between cytokines, pyroptosis, and the TME, elucidating their contribution to tumor progression and metastasis. By synthesizing emerging therapeutic targets and innovative technologies concerning TME, this review aims to provide novel insights that could enhance treatment outcomes for cancer patients.

中文翻译：

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肿瘤微环境中焦亡和细胞因子的串扰：从机制到临床意义


在癌症研究领域，肿瘤微环境 （TME） 在肿瘤的发生和发展中起着至关重要的作用，由癌细胞与周围非癌细胞之间的复杂相互作用形成。细胞因子作为必需的免疫调节剂，由 TME 内的各种细胞成分分泌，包括免疫细胞、癌症相关成纤维细胞和癌细胞本身。这些细胞因子促进了复杂的通信网络，从而显著影响肿瘤的发生、进展、转移和免疫抑制。细胞焦亡通过促进促炎细胞因子的释放和维持慢性炎症来促进 TME 重塑，从而影响免疫逃逸和血管生成等过程。然而，由于细胞因子、细胞焦亡和 TME 之间复杂的相互作用，以及细胞焦亡对癌症进展和治疗相关并发症（如细胞因子释放综合征）的双重影响，挑战仍然存在。解开这些复杂性可以促进平衡炎症反应的策略，同时最大限度地减少治疗期间的组织损伤。本综述深入探讨了细胞因子、焦亡和 TME 之间的复杂串扰，阐明了它们对肿瘤进展和转移的贡献。通过综合有关 TME 的新兴治疗靶点和创新技术，本综述旨在提供新的见解，以改善癌症患者的治疗结果。