Jalali Aliea M, Mitchell Kenyon J, Pompoco Christian, Poludasu Sudeep, Tran Sabrina, Ramana Kota V
Department of Biomedical Sciences, Noorda College of Osteopathic Medicine, Provo, UT 84606, USA.
Int J Mol Sci. 2024 Dec 21;25(24):13689. doi: 10.3390/ijms252413689.
Besides various infectious and inflammatory complications, recent studies also indicated the significance of NLRP3 inflammasome in cancer progression and therapy. NLRP3-mediated immune response and pyroptosis could be helpful or harmful in the progression of cancer, and also depend on the nature of the tumor microenvironment. The activation of NLRP3 inflammasome could increase immune surveillance and the efficacy of immunotherapy. It can also lead to the removal of tumor cells by the recruitment of phagocytic macrophages, T-lymphocytes, and other immune cells to the tumor site. On the other hand, NLRP3 activation can also be harmful, as chronic inflammation driven by NLRP3 supports tumor progression by creating an environment that facilitates cancer cell proliferation, migration, invasion, and metastasis. The release of pro-inflammatory cytokines such as IL-1β and IL-18 can promote tumor growth and angiogenesis, while sustained inflammation may lead to immune suppression, hindering effective anti-tumor responses. In this review article, we discuss the role of NLRP3 inflammasome-mediated inflammatory response in the pathophysiology of various cancer types; understanding this role is essential for the development of innovative therapeutic strategies for cancer growth and spread.
除了各种感染性和炎症性并发症外，最近的研究还表明NLRP3炎性小体在癌症进展和治疗中具有重要意义。NLRP3介导的免疫反应和细胞焦亡在癌症进展中可能有益或有害，这也取决于肿瘤微环境的性质。NLRP3炎性小体的激活可以增强免疫监视和免疫治疗的疗效。它还可以通过招募吞噬性巨噬细胞、T淋巴细胞和其他免疫细胞到肿瘤部位来导致肿瘤细胞的清除。另一方面，NLRP3激活也可能有害，因为NLRP3驱动的慢性炎症通过创造一个促进癌细胞增殖、迁移、侵袭和转移的环境来支持肿瘤进展。促炎细胞因子如IL-1β和IL-18的释放可以促进肿瘤生长和血管生成，而持续的炎症可能导致免疫抑制，阻碍有效的抗肿瘤反应。在这篇综述文章中，我们讨论了NLRP3炎性小体介导的炎症反应在各种癌症类型病理生理学中的作用；了解这一作用对于开发针对癌症生长和扩散的创新治疗策略至关重要。
