细胞焦亡的生物学机制及其在乳腺癌中的研究进展

细胞焦亡是一种新近发现的促炎程序性死亡方式，细胞焦亡是由半胱天冬氨酸蛋白酶-1（Caspase-1）介导，通过GSDM家族蛋白的剪切活化，令细胞膜上形成小孔，从而使胞膜快速裂解，导致细胞内炎性内容物释放引起炎性反应的过程。细胞焦亡的三种途径分别为Caspase-1作用的经典通路、Caspase-4、5、11作用的非经典通路以及Caspase-3或Hela细胞作用的特殊通路。细胞焦亡在乳腺癌的发生、侵袭和转移方面起着重要的作用，与乳腺癌的预防和治疗有着密切的联系。本文就细胞焦亡的生物学机制及其在乳腺癌中的研究进展作一综述，以期为临床医生治疗乳腺癌提供新的思路。

Biological Mechanism of Pyroptosis and Its Research Progress in Breast Cancer

Pyroptosis is a newly discovered way of proinflammatory programmed cell death. Pyroptosis is mediated by caspase-1 (Caspase-1). Through the cleavage and activation of GSDM family proteins, small pores are formed on the cell membrane, thus rapid lysis of the cell membrane process, and then leads to intracellular inflammatory content release thereby causing inflammatory response. The three pyroptosis pathways are the classical pathway of Caspase-1, the non-classical pathway of Caspase-4, 5, and 11, and the special pathway of Caspase-3 or Hela cells. Pyroptosis plays an important role in the occurrence, invasion, and metastasis of breast cancer, and is closely related to the prevention and treatment of breast cancer. This article reviews the biological mechanism of pyroptosis and its research progress in breast cancer, to provide a new idea for clinicians in the treatment of breast cancer.