Possible therapeutic targets for NLRP3 inflammasome-induced breast cancer

作者：Xixi Wang, Junyi Lin, Zhe Wang, Zhi Li, Minghua Wang · 发表于：Discover Oncology · 年份：2023 · DOI：10.1007/s12672-023-00701-7 · 被引用次数：18 · 研究领域：Inflammasome and immune disorders、IL-33, ST2, and ILC Pathways

Inflammation plays a major role in the development and progression of breast cancer(BC). Proliferation, invasion, angiogenesis, and metastasis are all linked to inflammation and tumorigenesis. Furthermore, tumor microenvironment (TME) inflammation-mediated cytokine releases play a critical role in these processes. By recruiting caspase-1 through an adaptor apoptosis-related spot protein, inflammatory caspases are activated by the triggering of pattern recognition receptors on the surface of immune cells. Toll-like receptors, NOD-like receptors, and melanoma-like receptors are not triggered. It activates the proinflammatory cytokines interleukin (IL)-1β and IL-18 and is involved in different biological processes that exert their effects. The Nod-Like Receptor Protein 3 (NLRP3) inflammasome regulates inflammation by mediating the secretion of proinflammatory cytokines and interacting with other cellular compartments through the inflammasome's central role in innate immunity. NLRP3 inflammasome activation mechanisms have received much attention in recent years. Inflammatory diseases including enteritis, tumors, gout, neurodegenerative diseases, diabetes, and obesity are associated with abnormal activation of the NLRP3 inflammasome. Different cancer diseases have been linked to NLRP3 and its role in tumorigenesis may be the opposite. Tumors can be suppressed by it, as has been seen primarily in the context of colorectal cancer associated with colitis. However, cancers such as gas...