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

## TL;DR

This paper explores how EMT and inflammasome signaling interact in cancer and benign diseases, offering new therapeutic opportunities.

## Contribution

The paper provides mechanistic insights into the crosstalk between EMT and inflammasome signaling and highlights its therapeutic potential.

## Key findings

- EMT and inflammasome signaling create self-perpetuating mechanisms of cellular plasticity.
- Targeting inflammasomes like NLRP3 may inhibit metastasis and drug resistance.
- The EMT-inflammasome axis is context-dependent, influenced by cancer type and tumor microenvironment.

## Abstract

Epithelial-mesenchymal transition (EMT) and inflammasome signalling are intercon-nected processes which underpin tumour progression, metastasis, and therapeutic re-sistance. 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 mes-enchymal traits crucial for EMT. EMT transcriptional programmes can then in turn modulate the inflammasome via NF-κB/TGF-β signalling, creating self-perpetuating mechanisms of cellular plasticity and dysregulated therapeutic response. We have re-viewed the mechanistic evidence for EMT–inflammasome crosstalk in cancer and discussed the potential therapeutic implications. The function of the EMT-inflammasome axis is clearly context-dependent, with the cancer type, stage, and the complexity of the tumour microenvironment heavily contributing. The crosstalk between EMT and the inflammasome is an overlooked mechanism of tumour evolution, and targeting inflammasomes like NLRP3, or their downstream signalling pathways, offers a promising therapeutic avenue, with the objective of inhibiting metastasis and overcoming drug resistance.