Targeting EIF3C to suppress the development and progression of nasopharyngeal carcinoma

Abstract

Nasopharyngeal carcinoma occurs in many parts of the pars nasalis pharyngis, and the pathological type is mainly squamous cell carcinoma. Because of the special position of nasopharynx, breathing, pronunciation and daily life will be seriously affected. At present, the research direction of nasopharyngeal carcinoma is mainly to explore the law of tumor cell proliferation and migration, study the molecular mechanism, master its biological behavior and clinical significance, try to find therapeutic targets, and further improve the level of tumor treatment. However, the pathologic structure and molecular mechanism of nasopharyngeal carcinoma have not been fully elucidated. In this study, the Lentivirus-mediated EIF3C shRNA vector (L.V-shEIF3C) was constructed to down-regulate the expression of EIF3C in human pharyngeal squamous carcinoma cell FaDu and the human nasopharyngeal carcinoma cell 5-8F, it was found that down-regulation of EIF3C could significantly inhibit the cell proliferation, promote cell apoptosis, induce cell cycle arrest, and inhibit the formation and growth of tumors in mouse models. This study provides strong evidence that EIF3C is a key gene driving the development and progression of head and neck cancer, which is of great significance for the diagnosis, prognosis or treatment of tumors, suggesting that EIF3C may become a valuable therapeutic development and intervention target.

A novel EIF3C-related CD8+ T-cell signature in predicting prognosis and immunotherapy response of nasopharyngeal carcinoma

“…So far, overexpressed EIF3C has been determined in a variety of tumors, such as ovarian cancer, colon cancer, renal cell carcinoma and cervical cancer, but few studies have mentioned NPC (Liu et al 2020 ; Song et al 2013 ; Fan et al 2019 ; Hu et al 2019 ). Zhao et al have investigated the role of EIF3C in NPC by examining the expression levels of genes in apoptosis-related signaling pathways, and discovered that downregulation of EIF3C made an impact on the expression of phosphorylated P44/p42 MAPK, phosphorylated AKT, and phosphorylated SMad2, promoting apoptosis of pharyngeal squamous carcinoma cells by downregulating these genes’ expression (Zhao et al 2022 ). However, there have been no research elucidating the regulatory role of EIF3C in the TIME and immunotherapy response prediction of NPC patients.…”

An innovative gene expression modulating strategy by converting nucleic acids into HNC therapeutics using carrier-free nanoparticles

“…This phenomenon can potentially be attributed to the abnormal expression of certain proteins in tumor cells, which consequently impairs immune cell functionality, leading to tumor immune evasion and immunosuppression ( 11 – 14 ). Noteworthily, the investigation of eukaryotic initiation factor 3c (eIF3C) as a potential antitumor target in the therapeutic exploration of HNC has been progressively undertaken ( 15 , 16 ). eIF3C, a constituent of the largest eukaryotic translation initiation factor eIF3 complex, plays a crucial role in regulating transcript-specific translation during development and exhibits elevated expression levels in various cancer types ( 15 , 17 , 18 ).…”

“…Noteworthily, the investigation of eukaryotic initiation factor 3c (eIF3C) as a potential antitumor target in the therapeutic exploration of HNC has been progressively undertaken ( 15 , 16 ). eIF3C, a constituent of the largest eukaryotic translation initiation factor eIF3 complex, plays a crucial role in regulating transcript-specific translation during development and exhibits elevated expression levels in various cancer types ( 15 , 17 , 18 ). Suppression of eIF3C results in disruption of translation initiation complexes and decreased protein expressions, leading to cell cycle arrest and apoptosis ( 15 , 16 , 19 ).…”

“…eIF3C, a constituent of the largest eukaryotic translation initiation factor eIF3 complex, plays a crucial role in regulating transcript-specific translation during development and exhibits elevated expression levels in various cancer types ( 15 , 17 , 18 ). Suppression of eIF3C results in disruption of translation initiation complexes and decreased protein expressions, leading to cell cycle arrest and apoptosis ( 15 , 16 , 19 ). Nevertheless, similar to other tumor-specific proteins and associated PPIs, inhibiting eIF3C through direct protein-level regulation poses significant challenges.…”