Journal of Oral Science Research ›› 2024, Vol. 40 ›› Issue (9): 803-809.DOI: 10.13701/j.cnki.kqyxyj.2024.09.009

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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

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