Abstract：
BACKGROUND: 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.
METHODS: 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.
RESULTS: 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).
CONCLUSIONS: 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.
METHODS: 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.
RESULTS: 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).
CONCLUSIONS: 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.
摘要：
背景：驱动蛋白家族成员26B（KIF26B）与多种肿瘤的发生和进展密切相关。然而,关于其在口腔鳞状细胞癌（OSCC）中的作用的研究有限。本文旨在研究KIF26B在OSCC中的表达水平及其机制。
方法：进行实时定量聚合酶链反应（RT-qPCR）和Westernblot分析，以评估35例OSCC标本及其相应的非癌组织中KIF26B的表达水平。在HSC6和SCC25细胞中实现KIF26B的过表达和沉默，分别,导致KIF26B过表达和si-KIF26B细胞系的建立，指定为KIF26B组和si-KIF26B组。使用5-乙炔基-2'-脱氧尿苷（EdU）标记和克隆形成进行增殖测定，以评估这些组中细胞的增殖能力。使用Transwell测定法评估KIF26B和si-KIF26B组中的细胞的侵入和迁移能力。此外,通过Westernblot分析KIF26B对糖原合成酶激酶（GSK）-3β/β-catenin通路的影响。
结果：根据RT-qPCR和Westernblot分析的结果，OSCC组织中KIF26B的表达明显高于正常组织(p<0.01)。KIF26B的过表达显著加速了细胞迁移，入侵,和增殖（p<0.01），而KIF26B的敲减显着抑制了这些过程（p<0.01）。此外,KIF26B过表达导致活性β-连环蛋白水平升高，p-GSK-3和c-myc(p<0.01)，而KIF26B沉默降低了这些蛋白质的水平(p<0.01)。
结论：我们的研究结果表明，KIF26B可能作为癌基因在OSCC的发病和进展中发挥作用。本研究为确定OSCC的潜在治疗靶点奠定了基础。
方法：进行实时定量聚合酶链反应（RT-qPCR）和Westernblot分析，以评估35例OSCC标本及其相应的非癌组织中KIF26B的表达水平。在HSC6和SCC25细胞中实现KIF26B的过表达和沉默，分别,导致KIF26B过表达和si-KIF26B细胞系的建立，指定为KIF26B组和si-KIF26B组。使用5-乙炔基-2'-脱氧尿苷（EdU）标记和克隆形成进行增殖测定，以评估这些组中细胞的增殖能力。使用Transwell测定法评估KIF26B和si-KIF26B组中的细胞的侵入和迁移能力。此外,通过Westernblot分析KIF26B对糖原合成酶激酶（GSK）-3β/β-catenin通路的影响。
结果：根据RT-qPCR和Westernblot分析的结果，OSCC组织中KIF26B的表达明显高于正常组织(p<0.01)。KIF26B的过表达显著加速了细胞迁移，入侵,和增殖（p<0.01），而KIF26B的敲减显着抑制了这些过程（p<0.01）。此外,KIF26B过表达导致活性β-连环蛋白水平升高，p-GSK-3和c-myc(p<0.01)，而KIF26B沉默降低了这些蛋白质的水平(p<0.01)。
结论：我们的研究结果表明，KIF26B可能作为癌基因在OSCC的发病和进展中发挥作用。本研究为确定OSCC的潜在治疗靶点奠定了基础。
