TTK Defines a High-Risk Oral Squamous Cell Carcinoma Subtype Through Dual mTORC1/NF-κB Activation

Our findings establish TTK as a pivotal mediator defining a high-risk OSCC molecular subtype characterized by simultaneous activation of the mTORC1 and NF-κB pathways and severe genomic instability. The discovery of a direct interaction between TTK and the TAK1-TAB complex provides novel mechanistic insight into NF-κB activation, while its inhibition significantly improves cisplatin sensitivity. These results warrant further clinical evaluation of TTK inhibitors as a promising therapeutic strategy to improve outcomes in aggressive OSCC.