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

ABSTRACT:

Background

Gastrointestinal neuroendocrine tumors (GI-NETs) are rare neoplasms with limited therapeutic options and increasing clinical incidence. Focal adhesion kinase (FAK) has been implicated in oncogenic processes across various tumor types; however, its specific role in GI-NET biology remains inadequately characterized. This study investigates the impact of FAK inhibition on GI-NET cell survival, invasive potential, and gene regulation, with the aim of evaluating FAK as a therapeutic target.

Methods

Human GI-NET cell lines (GOT1 and COLO320DM) were treated with Y15, a kinase inhibitor, and PROTAC-FAK (BI-0319), a degrader that abrogates both enzymatic and scaffold functions. siRNA-mediated knockdown of FAK was employed for functional validation. Assays assessing viabili

SUBMITTER: Toffoli L 

PROVIDER: S-EPMC12358824 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature