Regulation of Inflammasome by microRNAs in Triple-Negative Breast Cancer: New Opportunities for Therapy

During the past decade, researchers have investigated the molecular mechanisms of breast cancer initiation and progression, especially triple-negative breast cancer (TNBC), in order to identify specific biomarkers that could serve as feasible targets for innovative therapeutic strategies development. TNBC is characterized by a dynamic and aggressive nature, due to the absence of estrogen, progesterone and human epidermal growth factor 2 receptors. TNBC progression is associated with the dysregulation of nucleotide-binding oligomerization domain-like receptor and pyrin domain-containing protein 3 (NLRP3) inflammasome, followed by the release of pro-inflammatory cytokines and caspase-1 dependent cell death, termed pyroptosis. The heterogeneity of the breast tumor microenvironment triggers the interest of non-coding RNAs' involvement in NLRP3 inflammasome assembly, TNBC progression and metastasis. Non-coding RNAs are paramount regulators of carcinogenesis and inflammasome pathways, which could help in the development of efficient treatments. This review aims to highlight the contribution of non-coding RNAs that support inflammasome activation and TNBC progression, pointing up their potential for clinical applications as biomarkers for diagnosis and therapy.

Automated summary

Researchers have studied the molecular mechanisms of breast cancer initiation and progression, particularly TNBC, to find specific biomarkers for innovative therapeutic strategies. TNBC is characterized by the absence of certain receptors, making it dynamic and aggressive. TNBC progression is associated with dysregulation of the NLRP3 inflammasome, leading to the release of pro-inflammatory cytokines and caspase-1 dependent cell death. Non-coding RNAs play a significant role in the assembly of the NLRP3 inflammasome, TNBC progression, and metastasis, offering potential for diagnosis and therapy.