Background/Objectives:Head and neck cancer (HNC) is among the most common cancer types globally, with its incidence expected to increase significantly in the coming years. Oral squamous cell carcinoma (OSCC), the predominant subtype, exhibits significant heterogeneity and resistance to treatment. Current therapies, including surgery, radiation, and chemotherapy, often result in poor outcomes for advanced stages. Cetuximab, an EGFR inhibitor, is widely used but faces limitations. This study explores the combined inhibition of EGFR and mitotic proteins to enhance treatment efficacy.Methods:We analyzed the effects of co-treating OSCC cells with small molecules targeting MPS-1 (BAY1217389), Aurora-B (Barasertib), or KSP (Ispinesib), alongside Cetuximab. The rationale is based on targeting EGFR-mediated survival pathways and the mitotic checkpoint, addressing multiple cell cycle phases and reducing resistance.Results:Our findings indicate that inhibiting MPS-1, Aurora-B, or KSP enhances Cetuximab’s therapeutic potential, promoting increased cancer cell death. Additionally, we examined EGFR, MPS-1, Aurora-B, and KSP expression in OSCC patient samples, revealing their clinicopathologic significance.Conclusions:This combinatorial approach suggests a promising strategy to improve treatment outcomes in OSCC.
**背景/目的：** 头颈癌是全球最常见的癌症类型之一，其发病率预计在未来几年将显著上升。口腔鳞状细胞癌作为其主要亚型，表现出显著的异质性和治疗抵抗性。目前针对晚期患者的治疗手段，包括手术、放疗和化疗，往往效果不佳。西妥昔单抗作为一种表皮生长因子受体抑制剂虽广泛应用，但存在局限性。本研究旨在探索联合抑制EGFR和有丝分裂相关蛋白，以提升治疗效果。 **方法：** 我们分析了使用靶向MPS-1（BAY1217389）、Aurora-B（Barasertib）或KSP（Ispinesib）的小分子药物与西妥昔单抗联合处理OSCC细胞的效果。其理论基础在于同时靶向EGFR介导的生存通路和有丝分裂检查点，以作用于多个细胞周期阶段并降低耐药性。 **结果：** 我们的研究结果表明，抑制MPS-1、Aurora-B或KSP能增强西妥昔单抗的治疗潜力，促进癌细胞死亡增加。此外，我们检测了OSCC患者样本中EGFR、MPS-1、Aurora-B和KSP的表达情况，揭示了其临床病理学意义。 **结论：** 这种联合治疗方案为提高OSCC的治疗效果提供了一种具有前景的策略。
肿瘤(癌症)患者之家