本研究旨在探究降胆固醇药物辛伐他汀在抑制口腔鳞状细胞癌（OSCC）中的作用及具体机制。采用CCK8法、定量实时聚合酶链反应（qPCR）、蛋白质印迹、克隆形成实验、TdT介导的dUTP末端连接酶标记、划痕愈合实验检测OSCC细胞的增殖、凋亡和迁移水平。通过小鼠异种移植瘤模型检测了辛伐他汀在体内的抑制作用。采用免疫组织化学和免疫荧光染色评估了细胞和组织中的KLF2和β-连环蛋白表达。OSCC细胞和组织中KLF2的表达下调。KLF2诱导剂GGTI298的添加抑制了OSCC细胞的增殖和迁移。辛伐他汀在抑制OSCC细胞的增殖和促进凋亡方面发挥了作用。此外，它还抑制了OSCC细胞中的β-连环蛋白表达并促进了KLF2的表达。KLF2 siRNA逆转了辛伐他汀对OSCC细胞增殖和凋亡的影响。作为肿瘤抑制基因，KLF2可能是诊断和治疗OSCC的重要标志物。辛伐他汀通过调节KLF2信号抑制了OSCC的进展。版权所有 © 2023. Elsevier B.V.发表。

This study aimed to explore the role and specific mechanism of the cholesterol-lowering drug simvastatin in inhibiting oral squamous cell carcinoma (OSCC).The proliferation, apoptosis, and migration levels of OSCC cells were detected by CCK8, quantitative real-time polymerase chain reaction, western blot, colony formation, TdT-mediated dUTP Nick-End Labeling assay, and wound healing assay. The inhibitory effect of simvastatin in vivo was detected by a mouse xenograft tumor model. Immunohistochemistry and immunofluorescence staining were used to assess the KLF2 and β-catenin expressions in cells and tissues.KLF2 expression in OSCC cells and tissues was downregulated. The addition of KLF2 inducer, GGTI298, inhibited the proliferation and migration of OSCC cells. Simvastatin played a role in inhibiting the proliferation and promoting the apoptosis of OSCC cells. Moreover, it inhibited β-catenin expression and promoted KLF2 expression in OSCC cells. KLF2 siRNA reversed the effect of simvastatin on the proliferation and apoptosis of OSCC cells.KLF2, as a tumor suppressor gene, may be an important marker for diagnosing and treating OSCC. Simvastatin inhibits the progression of OSCC by regulating the KLF2 signal.Copyright © 2023. Published by Elsevier B.V.