FERMT1 expression

FERMT1 was highly expressed in NSCLC and can activate the p38 MAPK signaling pathway through up-regulation of PKP3, thus promoting the invasion and migration of NSCLC.

Finally, FERMT1 overexpression may be sensitive to chemotherapy drugs such as Palbociclib, AM-5992 and TAE-226. FERMT1 can serve as a diagnostic and prognostic marker of PAAD, which is connected with immune cell infiltration and the modulation of mA and necroptosis.

The DEG profiles between tissues from TNBC and other subtypes of breast cancer were identified using RNA-sequencing and bioinformatics analysis. FERMT1 was significantly upregulated in TNBC tumor tissues, and increased expression of FERMT1 was associated with poor OS of TNBC patients. FERMT1 could serve as a specific biomarker of and therapeutic target in TNBC.

These data indicated that FERMT1 could be a good potential therapeutic target for NPC treatment.

In the present study, we introduced KINDLIN1 as a location-specific marker for cardia gastric carcinoma. Moreover, it was observed that KINDLIN1 could be used as a gender-dependent diagnostic marker of GC patients.

FERMT1 silencing inhibits the migration, invasion, and EMT of OSCC cells via inactivation of the PI3K/AKT signaling pathway, suggesting that FERMT1 is a novel and potential therapeutic target for anti-metastatic strategies for OSCC.

The research provides a new perspective on the distinct roles of Kindlins in NSCLC and likely has important implications for future novel biomarkers and therapeutic targets in NSCLC.

Furthermore, FERMT1 enhancement reversed circ_0000554 inhibition-mediated effects on the colony formation, migration, invasion, radiosensitivity and apoptosis of esophageal cancer cells. Circ_0000554 silencing repressed EC progression and enhanced cell radiosensitivity through downregulating FERMT1 via sponging miR-485-5p, which provided a possible method for improving the radioresistence of esophageal cancer.

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.