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.

炎症和癌变是紧密相关的过程，不仅因为炎症会促进DNA不稳定，而且因为这两个过程都是由NF-kB，STAT3，mTOR和MAPKs等途径驱动的。有趣的是，这些途径调节促炎性细胞因子（如IL-6，TNF-α和IL-1β）的释放，进而控制其激活并在塑造免疫应答中起关键作用。转录因子p53是主要的肿瘤抑制因子，经常在癌症中发生突变，从而促进肿瘤的进展。在本概述中，我们强调了促炎细胞因子与促炎/促癌途径之间的相互作用，如何通过UPR信号转导和自噬进行调节和调节，如何影响mutp53的稳定性，进而能够控制自噬，UPR信号转导，细胞因子的释放和激活相同的致癌途径，以保持自身的稳定性并促进肿瘤发生。中断这些正反馈回路可能代表抗癌治疗中有希望的策略，尤其是针对携带mutp53的癌症。