%0 Journal Article
%T Identification of KIF26B as a Tumor Marker for Oral Squamous Cell Carcinoma.
%A Li Q
%A Zhan X
%A Tan Y
%J Discov Med
%V 36
%N 185
%D 2024 Jun
%M 38926114
%F 3.222
%R 10.24976/Discov.Med.202436185.118
%X <B>BACKGROUND: </B>Kinesin family member 26B (KIF26B) has been closely linked to the occurrence and progression of various tumors. However, there is limited research on its role in oral squamous cell carcinoma (OSCC). This article aims to investigate the expression levels and mechanisms of KIF26B in OSCC.<BR><B>METHODS: </B>Real time quantity polymerase chain reaction (RT-qPCR) and Western blot analyses were conducted to assess the expression levels of KIF26B in 35 OSCC specimens and their corresponding non-cancerous tissues. Overexpression and silencing of KIF26B were achieved in HSC6 and SCC25 cells, respectively, resulting in the establishment of KIF26B-overexpressing and si-KIF26B cell lines, designated as the KIF26B group and si-KIF26B group. Proliferation assays using 5-Ethynyl-2'-deoxyuridine (EdU) labeling and clone formation were performed to evaluate the proliferative capacity of cells in these groups. The invasive and migratory abilities of cells in the KIF26B and si-KIF26B groups were assessed using Transwell assay. Additionally, the influence of KIF26B on the glycogen synthase kinase (GSK)-3β/β-catenin pathway was investigated through Western blot analysis.<BR><B>RESULTS: </B>According to the results of RT-qPCR and Western blot analyses, the expression of KIF26B was predominantly higher in OSCC tissues compared to normal tissues (p < 0.01). Overexpression of KIF26B notably accelerated cell migration, invasion, and proliferation (p < 0.01), whereas knockdown of KIF26B significantly inhibited these processes (p < 0.01). Additionally, KIF26B overexpression led to increased levels of active β-catenin, p-GSK-3, and c-myc (p < 0.01), while KIF26B silencing decreased the levels of these proteins (p < 0.01).<BR><B>CONCLUSIONS: </B>Our findings suggest that KIF26B may play a role in the pathogenesis and progression of OSCC as an oncogene. This study establishes a foundation for the identification of potential therapeutic targets for OSCC.