Wang Xixi, Lin Junyi, Wang Zhe, Li Zhi, Wang Minghua
Department of General Surgery, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, China.
Sinopharm Dongfeng General Hospital, Hubei University of Medicine, Shiyan, 442000, China.
Discov Oncol. 2023 Jun 10;14(1):93. doi: 10.1007/s12672-023-00701-7.
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 gastric and skin can also be promoted by it. The inflammasome NLRP3 is associated with breast cancer, but there are few specific reviews. This review focuses on the structure, biological characteristics and mechanism of inflammasome, the relationship between NLRP3 in breast cancer Non-Coding RNAs, MicroRNAs and breast cancer microenvironment, especially the role of NLRP3 in triple-negative breast cancer (TNBC). And the potential strategies of using NLRP3 inflammasome to target breast cancer, such as NLRP3-based nanoparticle technology and gene target therapy, are reviewed.
炎症在乳腺癌（BC）的发生和发展中起主要作用。增殖、侵袭、血管生成和转移都与炎症和肿瘤发生有关。此外，肿瘤微环境（TME）炎症介导的细胞因子释放在这些过程中起关键作用。通过衔接蛋白凋亡相关斑点蛋白招募半胱天冬酶-1，炎症半胱天冬酶通过免疫细胞表面模式识别受体的触发而被激活。Toll样受体、NOD样受体和黑色素瘤样受体未被触发。它激活促炎细胞因子白细胞介素（IL）-1β和IL-18，并参与发挥其作用的不同生物学过程。Nod样受体蛋白3（NLRP3）炎性小体通过介导促炎细胞因子的分泌并通过炎性小体在固有免疫中的核心作用与其他细胞区室相互作用来调节炎症。近年来，NLRP3炎性小体激活机制备受关注。包括肠炎、肿瘤、痛风、神经退行性疾病、糖尿病和肥胖在内的炎症性疾病与NLRP3炎性小体的异常激活有关。不同的癌症疾病与NLRP3有关，其在肿瘤发生中的作用可能相反。它可以抑制肿瘤，这主要见于与结肠炎相关的结直肠癌中。然而，胃癌和皮肤癌等癌症也可能由它促进。炎性小体NLRP3与乳腺癌有关，但具体综述较少。本综述重点关注炎性小体的结构、生物学特性和机制，NLRP3在乳腺癌非编码RNA、微小RNA与乳腺癌微环境之间的关系，尤其是NLRP3在三阴性乳腺癌（TNBC）中的作用。并综述了利用NLRP3炎性小体靶向乳腺癌的潜在策略，如基于NLRP3的纳米颗粒技术和基因靶向治疗。
