TRIP13 Promotes Hypopharyngeal Cancer Progression

Abstract

Background: Hypopharyngeal cancer (HPC) is a prevalent malignancy commonly occurring in the head and neck region, with a five-year survival rate ranging from 30–50%. Consequently, there is an urgent need to delve into the underlying molecular mechanisms and to identify novel biomarkers that can serve as therapeutic targets for treating HPC. Methods: The GSE2379 dataset and HPC data in The Cancer Genome Atlas (TCGA) database were utilized for combination bioinformatics analysis. The mRNA and protein expression levels of thyroid hormone receptor interactor 13 (TRIP13) were evaluated both in vitro and in vivo, as well as in clinical samples using quantitative real-time polymerase chain reaction (qRT-PCR) and western blot (WB) analysis. Furthermore, the malignant phenotypes of HPC cells were assessed employing the Transwell, wound healing, and flow cytometry assays. A xenograft tumor nude mice model was established to observe the tumor growth and lung metastases. Moreover, the role of TRIP13 in regulating the mitogen-activated protein kinase (MAPK) pathway was assessed using bioinformatic analysis. Results: Our analysis revealed the participation of 66 common up-regulated differential expressed genes (DEGs) in the epithelial-mesenchymal transition (EMT) related signaling pathway. Furthermore, TRIP13 level was elevated in FaDu cells, xenograft tumor nude mice, and clinical HPC samples. The knocking down of TRIP13 suppressed the invasion, migration, and cell cycle of FaDu cells in vitro, and inhibited tumor growth, lung metastases, and pathological conditions in vivo. Conclusion: This study reveals the role of TRIP13, as a potential oncogene, in promoting the development of HPC.