Rho GTP 酶激活蛋白 11A (ARHGAP11A) 可促进 RhoA 中的 GTP 水解。 ARHGAP11A 在口腔鳞状细胞癌 (OSCC) 中的功能尚未被探索。本研究旨在研究 OSCC 中 ARHGAP11A 的表达谱、其与患者预后的相关性、其对细胞周期进展的影响以及其失调的机制。使用来自癌症基因组图谱-Head 和癌症基因组图谱的数据进行生物信息学分析。颈部鳞状细胞癌（TCGA-HNSC）。使用携带 ARHGAP11A shRNA 的慢病毒来确定 ARHGAP11A 敲低对肿瘤细胞增殖和细胞周期进展的影响。利用双荧光素酶报告基因检测来检查 FOXM1 如何转录调节 ARHGAP11A 表达。ARHGAP11A 上调与 TSCC 患者不利的总生存 (OS) 相关（HR：2.142，95%CI：1.224-3.749，P = 0.007），但不适用于舌头以外部位的 OSCC 患者。 ARHGAP11A 敲低可抑制 TSCC 细胞的体外和体内增殖，并诱导 G1 期停滞。 ARHGAP11A 敲除增加了 GTP-RhoA，但降低了 p-RB 水平，但不影响 RhoA 和 RB 的总表达。 ARHGAP11A 敲除增加了 p27 的表达并减少了细胞周期蛋白 E1 的表达。 ARHGAP11A 在 TSCC 细胞中通过启动子区域的多个 FOXM1 结合位点被 FOXM1 转录激活。这项研究揭示了 ARHGAP11A 在 TSCC 中的致癌作用，强调了其对细胞周期控制和肿瘤增殖的影响。此外，FOXM1 和 ARHGAP11A 之间的调控关系为 TSCC 中的转录网络提供了新的见解。© 2024 中华民国牙科科学协会。 Elsevier B.V. 的出版服务

Rho GTPase activating protein 11A (ARHGAP11A) can facilitate GTP hydrolysis in RhoA. The functions of ARHGAP11A in oral squamous cell carcinoma (OSCC) have not yet been explored. This study aimed to investigate the expression profile of ARHGAP11A in OSCC, its correlation with patient prognosis, its effect on cell-cycle progression, and the mechanisms by which it is dysregulated.Bioinformatics analysis was conducted using data from The Cancer Genome Atlas-Head and Neck Squamous Cell Carcinoma (TCGA-HNSC). Lentiviruses carrying ARHGAP11A shRNAs were employed to determine the effects of ARHGAP11A knockdown on tumor cell proliferation and cell-cycle progression. Dual-luciferase reporter assays were utilized to examine how FOXM1 transcriptionally regulates ARHGAP11A expression.ARHGAP11A upregulation was associated with unfavorable overall survival (OS) in patients with TSCC (HR: 2.142, 95%CI: 1.224-3.749, P = 0.007), but not in patients with OSCC of sites other than the tongue. ARHGAP11A knockdown inhibited the proliferation of TSCC cells in vitro and in vivo, and induced G1 phase arrest. ARHGAP11A knockdown increased GTP-RhoA but decreased p-RB levels, while it did not affect the total expression of RhoA and RB. ARHGAP11A knockdown increased p27 and decreased cyclin E1 expression. ARHGAP11A is transcriptionally activated by FOXM1 via multiple FOXM1 binding sites in the promoter regions in TSCC cells.This study revealed the oncogenic role of ARHGAP11A in TSCC, highlighting its impact on cell-cycle control and tumor proliferation. Furthermore, the regulatory relationship between FOXM1 and ARHGAP11A provides new insights into the transcriptional networks in TSCC.© 2024 Association for Dental Sciences of the Republic of China. Publishing services by Elsevier B.V.