FAK inhibition disrupts tumor growth, apoptosis, and transcriptional regulation in GI-NETs

FAK inhibition impairs GI-NET viability, invasion, and colony formation in both 2D and 3D models using kinase (Y15) and PROTAC-based degraders (BI-0319).PROTAC-FAK uniquely reduces H3K9 acetylation, revealing a kinase-independent scaffold role for FAK in epigenetic regulation.esiRNA knockdown of FAK recapitulates pharmacological effects, confirming FAK as a driver of oncogenic features in GI-NET cells.In silico analysis identifies elevated PTK2 expression in rectal and small intestine NETs, with a strong positive correlation to RB1, supporting translational relevance.