Exploring the molecular mechanisms underlying the inflammation–cancer transformation in Hashimoto thyroiditis using single-cell transcriptomics

FECs specifically communicated with mast cells via the FN1/CD44 signaling axis. In vitro experiments further confirmed that, under inflammatory conditions, mast cells secreted IL-8, which activated the PI3K/AKT pathway and promoted malignant phenotypes. Collectively, these findings suggest that IL1B⁻ FECs recruit mast cells through the FN1/CD44 axis, and mast cell-derived IL-8 subsequently activates the PI3K/AKT pathway to drive the transformation from HT to PTC, providing novel mechanistic insights into the "inflammation-to-cancer" transition.