Xia Qing, Zhang Jingzhou
Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Peking Union Medical College, Graduate School of Peking Union Medical College, Beijing, China.
Cell Biochem Funct. 2025 Jan;43(1):e70035. doi: 10.1002/cbf.70035.
Autophagy is a physiologically regulated cellular process orchestrated by autophagy-related genes (ATGs) that, depending on the tumor type and stage, can either promote or suppress tumor growth and progression. It can also modulate cancer stem cell maintenance and immune responses. Therefore, targeted manipulation of autophagy may inhibit tumor development by overcoming tumor-promoting mechanisms. The inflammasome is another multifunctional bioprocess that induces a form of pro-inflammatory programmed cell death, called pyroptosis. Dysregulation or overactivation of the inflammasome has been implicated in tumor pathogenesis and development. Additionally, autophagy can inhibit the NLRP3 inflammasome by removing inflammatory drivers. Recent research suggests that the NLRP3 inflammasome, in turn, affects autophagy. Understanding the complex interplay between autophagy and inflammasomes could lead to more precise and effective strategies for cancer treatments. In this review, we summarize the impact of autophagy and inflammasome dysregulation on tumor progression or suppression. We then highlight their targeting for cancer treatment as monotherapy or in combination with other therapies. Furthermore, we discuss the interaction between autophagy and tumor-promoting inflammation or the NLRP3 inflammasome. Finally, based on recent findings, we review the potential of this interaction for cancer treatment.
自噬是一种由自噬相关基因（ATG）精心编排的生理调节细胞过程，根据肿瘤类型和阶段，它既可以促进也可以抑制肿瘤生长和进展。它还可以调节癌症干细胞的维持和免疫反应。因此，对自噬进行靶向操控可能通过克服肿瘤促进机制来抑制肿瘤发展。炎性小体是另一种多功能生物过程，可诱导一种称为细胞焦亡的促炎性程序性细胞死亡形式。炎性小体的失调或过度激活与肿瘤发病机制和发展有关。此外，自噬可以通过清除炎症驱动因素来抑制NLRP3炎性小体。最近的研究表明，NLRP3炎性小体反过来又会影响自噬。了解自噬与炎性小体之间的复杂相互作用可能会带来更精确、有效的癌症治疗策略。在这篇综述中，我们总结了自噬和炎性小体失调对肿瘤进展或抑制的影响。然后，我们强调将它们作为单一疗法或与其他疗法联合用于癌症治疗的靶向性。此外，我们讨论了自噬与肿瘤促进性炎症或NLRP3炎性小体之间的相互作用。最后，基于最近的研究结果，我们综述了这种相互作用在癌症治疗中的潜力。
