FERMT1 contributes to the migration and invasion of nasopharyngeal carcinoma through epithelial-mesenchymal transition and cell cycle arrest

• Published in: Cancer cell international 2022-02, Vol.22 (1), p.70-70, Article 70
• Main Authors: Li, Lingling, Li, Piao, Zhang, Wei, Zhou, Haiting, Guo, Ergang, Hu, Guoqing, Zhang, Linli
• Format: Article
• Language: English
• Subjects: Antibodies; Apoptosis; Biotechnology; Cancer therapies; Cell adhesion & migration; Cell cycle; Cell cycle arrest; Cell growth; Cell migration; Cell proliferation; Cyclin-dependent kinases; Epithelial–mesenchymal transition; FERMT1; Flow cytometry; Gene expression; Immunohistochemistry; Immunoprecipitation; Kinases; Medical research; Mesenchyme; Metastasis; Motility; Nasopharyngeal carcinoma; NF-κB protein; Primary Research; Proteins; Reagents; Signal transduction; Therapeutic targets; Throat cancer; Tumorigenesis; Western blotting; Wound healing; Xenografts
• ISSN: 1475-2867; 1475-2867
• DOI: 10.1186/s12935-022-02494-1

Fermitin family member 1 (FERMT1) is significantly overexpressed in human cancers and associated with poor prognosis, but its contributions to tumorigenesis and nasopharyngeal carcinoma (NPC) progression remain unclear. The public GEO database was examined to investigate the role of FERMT1. Immunohistochemistry (IHC) staining of FERMT1 was performed in NPC tissues to corroborate the results. Western blotting and qRT-PCR were performed to test the expression of related proteins and mRNAs. Cell counting kit-8 assay (CCK8 assay) and colony formation assays were carried out to investigate the association of FERMT1 expression with NPC cell proliferation. The wound healing assay and Transwell assay were used to detect the migration and invasion of NPC cells. Flow cytometric analysis was conducted to detect the cell cycle transition of NPC cells. Co-immunoprecipitation (Co-IP) was employed to identify the correlation of FEMRT1 and Nod-like receptor family protein 3 (NLRP3). Xenograft tumors were generated to investigate the effect of FERMT1 on the growth of NPC cells in vivo. Here, we found that FERMT1 was upregulated in NPC tissues and correlated with the clinicopathological characteristics of NPC patients. Moreover, knockdown of FERMT1 significantly decreased cell proliferation, migration and invasion by mediating epithelial-mesenchymal transition (EMT) and cell cycle arrest of NPC cells both in vitro and in vivo. Knockdown FERMT1 inhibited EMT through directly binding to the NLRP3 and inhibited NF-kB signaling pathway. These data indicated that FERMT1 could be a good potential therapeutic target for NPC treatment.