口腔医学研究

口腔医学研究 ›› 2024, Vol. 40 ›› Issue (9): 803-809.DOI: 10.13701/j.cnki.kqyxyj.2024.09.009

• 口腔颌面外科学研究 • 上一篇    下一篇

CENPF调控PI3K/AKT信号通路影响唾液腺腺样囊性癌进展

杨心怡1, 黄薇薇1, 黄丽1, 胡赟2*   

  1. 1.贵州医科大学口腔医学院 贵州 贵阳 550004;
    2.贵州医科大学附属口腔医院病理科 贵州 贵阳 550004
  • 收稿日期:2024-04-02 出版日期:2024-09-28 发布日期:2024-09-25
  • 通讯作者: *胡赟,E-mail:huyun0403@163.com
  • 作者简介:杨心怡(1998~),女,湖南人,硕士,研究方向:口腔颌面外科临床技能训练与研究。
  • 基金资助:
    贵州省卫健委科学技术基金项目(编号:gzwjwkj2020-1-174)

Impact of CENPF on Progression of Adenoid Cystic Carcinoma through Regulation of PI3K/AKT Signaling Pathway

YANG Xinyi1, HUANG Weiwei1, HUANG Li1, HU Yun2*   

  1. 1. School of Stomatology, Guizhou Medical University, Guiyang 550004, China;
    2. Department of Pathology, Stomatological Hospital of Guizhou Medical University, Guiyang 550004, China
  • Received:2024-04-02 Online:2024-09-28 Published:2024-09-25

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摘要： 目的:探讨着丝粒蛋白F(centromere protein F,CENPF)在腺样囊性癌(adenoid cystic carcinoma,ACC)发生发展中的作用和分子机制。方法:通过小干扰RNA转染敲低ACC细胞中的CENPF。通过细胞计数试剂盒(cell counting kit-8,CCK-8)、划痕实验和Transwell测定评估敲低CENPF对ACC细胞增殖、迁移、侵袭的影响;通过蛋白免疫印迹实验分析改变CENPF表达后ACC细胞中磷脂酰肌醇-3-激酶(phosphatidylinositol-3-kinase,PI3K) /丝氨酸/苏氨酸蛋白激酶(serine/threonine protein kinase,AKT)/哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)信号通路相关蛋白表达变化,通过CCK-8、划痕实验和Transwell 测定评估敲低CENPF联合PI3K抑制剂BKM-120对ACC细胞增殖、迁移、侵袭的影响。结果:敲低ACC-M中CENPF表达后,CCK-8实验证明其增殖能力减弱;划痕实验表明其迁移能力减弱,Transwell实验表明其侵袭能力减弱,PI3K/AKT通路关键蛋白p-PI3K、p-AKT和p-mTOR蛋白表达水平下降。在下调CENPF的ACC-M中加入PI3K 抑制剂,PI3K/AKT通路关键蛋白表达水平进一步下降。此外,加入PI3K 抑制剂后,CENPF下调的ACC-M增殖、迁移、侵袭能力较单纯下调CENPF的ACC-M进一步减弱。结论:CENPF通过调控PI3K/AKT信号通路参与ACC进展。

关键词: 着丝粒蛋白F, 腺样囊性癌, PI3K/AKT信号通路, 机制研究

Abstract: Objective: To investigate the role and molecular mechanisms of CENPF in the pathogenesis and development of adenoid cystic carcinoma (ACC). Methods: CENPF in ACC cells was knocked down by transfection with small interfering RNA (siRNA). The effects of CENPF knockdown on the proliferation, migration, and invasion of ACC cells were evaluated using CCK-8, scratch assay, and transwell assay, respectively. Changes in the activity of phosphatidylinositol-3-kinase/serine/threonine protein kinase/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway-related proteins in ACC cells after altering CENPF expression were analyzed by Western blot. Finally, the combined effect of CENPF knockdown and PI3K inhibitor BKM-120 on the proliferation, migration, and invasion of ACC cells was assessed using CCK-8, scratch assay, and transwell assay. Results: Knockdown of CENPF expression in ACC-M cells resulted in decreased proliferation, migration, and invasion abilities as demonstrated by CCK-8, scratch assay, and transwell assay, respectively. The expression levels of key proteins in the PI3K/AKT pathway, including p-PI3K, p-AKT, and p-mTOR, were reduced. Furthermore, the expression levels of these proteins further decreased when PI3K inhibitor was added to CENPF-knockdown ACC-M cells. Additionally, the proliferation, migration, and invasion abilities of ACC-M cells with CENPF knockdown were further weakened when PI3K inhibitor was added compared to CENPF knockdown alone. Conclusion: CENPF regulates the progression of ACC by modulating the PI3K/AKT signaling pathway.

Key words: centromere protein F, adenoid cystic carcinoma, PI3K/AKT signaling pathway, mechanistic study