FERMT1 promotes gastric cancer progression by activating the NF-κB pathway and predicts poor prognosis.

Recent studies have reported that FERMT1, a newly discovered adhesion protein, contributes to an aggressive phenotype in several solid malignancies. However, the function and regulatory mechanism of FERMT1 in gastric cancer remain unknown. We found that FERMT1 was overexpressed in gastric cancer tissues compared with normal tissues. Clinical data analysis indicated that the expression of FERMT1 correlated with the overall survival of gastric cancer patients. Patients with higher FERMT1 expression had lower survival rates than patients with lower FERMT1 expression. We established stable cell lines with FERMT1 knockdown and overexpression. In vitro and in vivo experiments indicated that knockdown of FERMT1 inhibited the proliferation, invasion, metastasis, and epithelial-mesenchymal transition of gastric cancer cells. Mechanistically, FERMT1 was found to activate NF-κB signaling by promoting the degradation of IκBα, thereby promoting gastric cancer. These results provide new evidence of the oncogenic effects of FERMT1 in gastric cancer and suggest that FERMT1 might be a promising target for gastric cancer treatment.