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

Abstract

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

FERMT1 Is a Prognostic Marker Involved in Immune Infiltration of Pancreatic Adenocarcinoma Correlating with m6A Modification and Necroptosis

“…FERMT1 is essential to maintain cell-matrix adhesion as an integrin-interacting protein. The overexpression of FERMT1 was found in multiple tumors such as colon cancer, gastric cancer, oral squamous cell carcinoma, and nasopharyngeal carcinoma, and has been associated with metastasis and poor prognosis [ 9 , 10 , 11 , 12 ]. FERMT1 was highly expressed in epithelial non-small-cell lung cancer (NSCLC), but not in neuroendocrine NSCLC.…”

“…As a member of Kindlins, fermitin family member 1 (FERMT1, also known as Kindlin-1) is related to Kindler syndrome (KS), a genetic disorder that mainly affects the skin and intestine [ 8 ]. Moreover, abnormal FERMT1 expression has been described in several cancers, including colon cancer [ 9 ], gastric cancer [ 10 ], oral squamous cell carcinoma [ 11 ] and nasopharyngeal carcinoma [ 12 ]. FERMT1 is considered to be involved in tumor proliferation, apoptosis, metastasis, and tumor angiogenesis [ 7 ].…”

Amplifying T cell‐mediated antitumor immune responses in nonsmall cell lung cancer through photodynamic therapy and anti‐PD1

“…DEGs analysis was performed using the DESeq. 2 software, and pairwise comparisons were analyzed using edgeR 15 . Genes meeting the criteria of a false discovery rate (FDR) ≤ 0.05 and a fold change ≥2 were identified as DEGs.…”

“…2 software, and pairwise comparisons were analyzed using edgeR. 15 Genes meeting the criteria of a false discovery rate (FDR) ≤ 0.05 and a fold change ≥2 were identified as DEGs. The clusterProfiler package was utilized to conduct functional enrichment analysis of module genes in specific Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways.…”

FERMT1 contributes to the progression of prostate cancer through the p53 pathway

“…Kindlin-1 is primarily located in the epidermis, although it is also expressed in the colon, stomach, and kidneys to a lesser extent 11 . A previous study found that FERMT1 is a central tumor driver in cutaneous epithelial cells 12 . Loss-of-function mutations of FERMT1 cause a rare and recessive genodermatosis known as Kindler syndrome, which increases the risk of developing squamous cell carcinomas 13 .…”