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.

最近的研究报告称，FERMT1 是一种新发现的粘附蛋白，有助于几种实体恶性肿瘤的侵袭性表型。然而，FERMT1在胃癌中的功能和调控机制尚不清楚。我们发现与正常组织相比，FERMT1 在胃癌组织中过表达。临床数据分析表明，FERMT1的表达与胃癌患者的总生存期相关。FERMT1 表达较高的患者的存活率低于 FERMT1 表达较低的患者。我们建立了具有 FERMT1 敲低和过表达的稳定细胞系。体外和体内实验表明，FERMT1 的敲低抑制了胃癌细胞的增殖、侵袭、转移和上皮间质转化。从机制上讲，发现 FERMT1 通过促进 IκBα 的降解来激活 NF-κB 信号，从而促进胃癌的发生。这些结果为 FERMT1 在胃癌中的致癌作用提供了新的证据，并表明 FERMT1 可能是胃癌治疗的一个有希望的靶点。