Jia Yuming, Wang Xin, Deng Yanli, Li Shengchao, Xu Xiaowu, Qin Yi, Peng Li
Department of Hepatobiliary Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Emergency Department, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
J Cancer. 2023 Jan 1;14(1):140-151. doi: 10.7150/jca.77965. eCollection 2023.
Cancer is an important cause of death worldwide. The main types of cancer treatment are still surgery, chemotherapy and radiotherapy, and immunotherapy is becoming an important cancer treatment. Pyroptosis is a type of programmed cell death that accompanies an inflammatory response. This paper reviews the recent research progress in pyroptosis in tumors. Pyroptosis has been observed since 1986 and until recently has been recognized as programmed cell death mediated by GSDM family proteins. The molecular pathway of pyroptosis depends on the inflammasome-mediated caspase-1/GSDMD pathway, which is the canonical pathway, and the caspase-4/5/11/GSDMD pathway, which is the noncanonical pathway. Other pathways include caspase3/GSDME. Pyroptosis is a double-edged sword that is closely related to the tumor immune microenvironment. On the one hand, pyroptosis produces a chronic inflammatory environment, promotes the transition of normal cells to tumor cells, helps tumor cells achieve immune escape, and promotes tumor growth and metastasis. On the other hand, some tumor cell treatments can induce pyroptosis, which is a nonapoptotic form of cell death. Additionally, pyroptosis releases inflammatory molecules that promote lymphocyte recruitment and enhance the immune system's ability to kill tumor cells. With the advent of immunotherapy, pyroptosis has been shown to enhance the antitumor efficacy of immune checkpoint inhibitors. Some antineoplastic agents, such as chemotherapeutic agents, can also exert antineoplastic effects through the pyroptosis pathway. Pyroptosis, which is a programmed cell death mode, has been the focus of research in recent years, and the relationship between pyroptosis, tumors and tumor immunity has attracted attention, but there are still some questions to be answered regarding the specific mechanism. Further study of pyroptosis would aid in developing new antitumor therapies and has great clinical prospects.
癌症是全球范围内重要的死亡原因。癌症的主要治疗类型仍然是手术、化疗和放疗，而免疫疗法正成为一种重要的癌症治疗方法。细胞焦亡是一种伴随炎症反应的程序性细胞死亡。本文综述了肿瘤细胞焦亡的最新研究进展。细胞焦亡自1986年被观察到，直到最近才被认为是由GSDM家族蛋白介导的程序性细胞死亡。细胞焦亡的分子途径取决于炎性小体介导的caspase-1/GSDMD途径（即经典途径）和caspase-4/5/11/GSDMD途径（即非经典途径）。其他途径包括caspase3/GSDME。细胞焦亡是一把双刃剑，与肿瘤免疫微环境密切相关。一方面，细胞焦亡产生慢性炎症环境，促进正常细胞向肿瘤细胞转变，帮助肿瘤细胞实现免疫逃逸，并促进肿瘤生长和转移。另一方面，一些肿瘤细胞治疗可诱导细胞焦亡，这是一种非凋亡形式的细胞死亡。此外，细胞焦亡释放炎性分子，促进淋巴细胞募集并增强免疫系统杀伤肿瘤细胞的能力。随着免疫疗法的出现，细胞焦亡已被证明可增强免疫检查点抑制剂的抗肿瘤疗效。一些抗肿瘤药物，如化疗药物，也可通过细胞焦亡途径发挥抗肿瘤作用。细胞焦亡作为一种程序性细胞死亡模式，近年来一直是研究热点，细胞焦亡、肿瘤和肿瘤免疫之间的关系已引起关注，但在具体机制方面仍有一些问题有待解答。对细胞焦亡的进一步研究将有助于开发新的抗肿瘤疗法，并具有广阔的临床前景。
