Possible therapeutic targets for NLRP3 inflammasome-induced breast cancer

Abstract

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.

Breast Cancer Treatment Using the Magneto-Hyperthermia Technique Associated with Omega-3 Polyunsaturated Fatty Acids’ Supplementation and Physical Training

“…BC represents a growing global concern, especially for the female population of working age. Its pathophysiology presents a series of challenges, including the need to identify new prevention and treatment strategies, aiming to improve patients’ quality of life affected by this disease [ 46 , 47 , 48 , 49 ]. Recent studies have provided promising evidence of the benefits of omega-3 supplementation and complementary therapies in combination with chemotherapy, radiotherapy, and surgical procedures for patients with BC [ 50 , 51 , 52 , 53 ].…”

NLRP3 Inflammasome Inhibitors for Antiepileptogenic Drug Discovery and Development

“…Moreover, dexamethasone-loaded ROS-responsive polymer nanoparticles prepared by a modified emulsion approach had a strong ability to inhibit the expression of NLRP3, caspase1, and IL-1 [204]. It has been reported that nanoparticles themself trigger NLRP3 inflammasome activation [205][206][207][208]. However, the formation of a protein corona layer on lipid NPs caused a significant reduction in NLRP3 inflammasome activation and controlled the toxicity, biodistribution, and cellular uptake [209].…”

NLRP3 Inflammasome Inhibitors for Antiepileptogenic Drug Discovery and Development

“…Moreover, dexamethasone-loaded ROS-responsive polymer nanoparticles prepared by a modified emulsion approach had a strongest ability to inhibit the expression of NLRP3, caspase1, and IL-1b [207]. It has been reported that nanoparticles itself trigger the NLRP3 inflammasome activation [208][209][210][211]. However, the formation of protein corona layer on lipid NPs caused a significant reduction in NLRP3 inflammasome activation and controls the toxicity, biodistribution, and cellular uptake [212].…”