Crosstalk Between Inflammasome Signalling and Epithelial-Mesenchymal Transition in Cancer: Mechanistic Insights, Context-Dependence, and Therapeutic Opportunities

Epithelial-mesenchymal transition (EMT) and inflammasome signaling are interconnected processes which underpin tumour progression, metastasis, and therapeutic resistance. Inflammasomes such as NLRP3 encourage pro-inflammatory states (IL-1β, IL-18, NF-κB) and the activation of signalling pathways like TGF-β that promote mesenchymal traits crucial for EMT. EMT transcriptional programs can then in turn modulate the inflammasome via NF-κB/TGF-β signaling, creating self-perpetuating mechanisms of cellular plasticity and dysregulated therapeutic response. We have reviewed the mechanistic evidence for EMT–inflammasome crosstalk in cancer and discussed the potential therapeutic implications. The function of the ENT-inflammasome axis is clearly context-dependent, with the cancer type, stage, and the complexity of the tumour microenvironment heavily contributing. The between EMT and the inflammasome is an overlooked mechanism of tumour evolution and targeting inflammasomes like NLRP3, or their downstream signalling pathways offer a promising therapeutic avenue, with the therapeutic objective of reducing metastasis and overcoming drug resistance.