Inflammation and cancerogenesis are strongly interconnected processes, not only because inflammation promotes DNA instability, but also because both processes are driven by pathways such as NF-kB, STAT3, mTOR and MAPKs. Interestingly, these pathways regulate the release of pro-inflammatory cytokines such as IL-6, TNF-α and IL-1β that in turn control their activation and play a crucial role in shaping immune response. The transcription factor p53 is the major tumor suppressor that is often mutated in cancer, contributing to tumor progression. In this overview, we highlight how the interplay between pro-inflammatory cytokines and pro-inflammatory/pro-oncogenic pathways, regulating and being regulated by UPR signaling and autophagy, affects the stability of mutp53 that in turn is able to control autophagy, UPR signaling, cytokine release and the activation of the same oncogenic pathways to preserve its own stability and promote tumorigenesis. Interrupting these positive feedback loops may represent a promising strategy in anticancer therapy, particularly against cancers carrying mutp53.

炎症和癌变是紧密关联的过程，不仅因为炎症会促进 DNA 不稳定，还因为这两个过程均由 NF-kB、STAT3、mTOR 和 MAPK 等通路驱动。有趣的是，这些途径调节促炎细胞因子（如 IL-6、TNF-α 和 IL-1β）的释放，进而控制它们的激活，并在形成免疫反应中发挥关键作用。转录因子 p53 是主要的肿瘤抑制因子，在癌症中经常发生突变，从而促进肿瘤进展。在本概述中，我们重点介绍促炎细胞因子和促炎/促癌途径之间的相互作用，调节 UPR 信号和自噬以及受其调节，如何影响 mutp53 的稳定性，而 mutp53 反过来又能够控制自噬、UPR 信号、细胞因子释放和相同致癌途径的激活，以保持其自身稳定性并促进肿瘤发生。中断这些正反馈循环可能代表抗癌治疗的一种有前途的策略，特别是针对携带 mutp53 的癌症。