Due to the sustained proliferative potential of cancer cells, inducing cell death is a potential strategy for cancer therapy. Paraptosis is a mode of cell death characterized by endoplasmic reticulum (ER) and/or mitochondrial swelling and cytoplasmic vacuolization, which is less investigated. Considerable evidence shows that paraptosis can be triggered by various chemical compounds, particularly in cancer cells, thus highlighting the potential application of this non-classical mode of cell death in cancer therapy. Despite these findings, there remain significant gaps in our understanding of the role of paraptosis in cancer. In this review, we summarize the current knowledge on chemical compound-induced paraptosis. The ER and mitochondria are the two major responding organelles in chemical compound-induced paraptosis, which can be triggered by the reduction of protein degradation, disruption of sulfhydryl homeostasis, overload of mitochondrial Ca²⁺, and increased generation of reactive oxygen species. We also discuss the stumbling blocks to the development of this field and the direction for further research. The rational use of paraptosis might help us develop a new paradigm for cancer therapy.

由于癌细胞具有持续增殖的潜力，诱导细胞死亡是癌症治疗的潜在策略。细胞凋亡是一种细胞死亡模式，其特征是内质网（ER）和/或线粒体肿胀和细胞质空泡化，但对此的研究较少。大量证据表明，多种化合物可以引发细胞凋亡，特别是在癌细胞中，从而凸显了这种非经典细胞死亡模式在癌症治疗中的潜在应用。尽管有这些发现，但我们对Paraptosis在癌症中的作用的理解仍然存在重大差距。在这篇综述中，我们总结了目前关于化合物诱导的细胞凋亡的知识。内质网和线粒体是化合物诱导的细胞凋亡的两个主要响应细胞器，其可由蛋白质降解的减少、巯基稳态的破坏、线粒体Ca ²⁺的超载以及活性氧的产生增加来触发。我们还讨论了该领域发展的障碍以及进一步研究的方向。合理使用Paraptosis可能有助于我们开发癌症治疗的新范例。