口腔医学研究 ›› 2026, Vol. 42 ›› Issue (6): 519-523.DOI: 10.13701/j.cnki.kqyxyj.2026.06.010

• 口腔颌面外科学研究 • 上一篇    下一篇

RHOT1通过调节线粒体转移影响口腔鳞状细胞癌细胞侵袭性

赵欣然1, 倪玥琪2, 程波1*   

  1. 1.武汉大学中南医院口腔科 湖北 武汉 430061;
    2.武汉大学口腔医院综合科 湖北 武汉 430079
  • 收稿日期:2026-01-26 出版日期:2026-06-28 发布日期:2026-06-23
  • 通讯作者: *程波,E-mail:chengbo@znhospital.cn
  • 作者简介:赵欣然(2000~),女,湖北人,硕士在读,研究方向:线粒体转移及其调控机制研究。

RHOT1 Influences Invasiveness of Oral Squamous Cell Carcinoma Cells by Regulating Mitochondrial Transfer

ZHAO Xinran1, NI Yueqi2, CHENG Bo1*   

  1. 1. Department of Stomatology, Zhongnan Hospital of Wuhan University, Wuhan 430061, China;
    2. Department of General Dentistry, School and Hospital of Stomatology, Wuhan University, Wuhan 430079, China
  • Received:2026-01-26 Online:2026-06-28 Published:2026-06-23

摘要: 目的:探讨线粒体转运蛋白1(Ras homolog family member T1,RHOT1)在口腔鳞状细胞癌细胞与巨噬细胞间线粒体转移中的作用及其对肿瘤能量代谢与恶性行为的影响。方法:构建携带线粒体示踪荧光蛋白的巨噬细胞及RHOT1敲低的SCC7细胞。通过流式细胞术与共聚焦显微镜定量检测线粒体转移,并通过细胞内能量含量检测、细胞增殖活性检测和划痕愈合实验评价肿瘤细胞的能量代谢、增殖和迁移能力。结果:RHOT1敲低显著抑制SCC7细胞摄取巨噬细胞线粒体。外源性线粒体可促进阴性对照组细胞的增殖活性及迁移能力,而在RHOT1敲低的细胞中未观察到类似变化。结论:RHOT1通过调控肿瘤细胞对巨噬细胞来源线粒体的摄取,从而影响其能量代谢与恶性行为。RHOT1可能成为调控肿瘤代谢与免疫交互的潜在靶点。

关键词: 线粒体转运蛋白1, 线粒体转移, 口腔鳞状细胞癌, 巨噬细胞, 能量代谢

Abstract: Objective: To investigate the role of the mitochondrial transport protein Ras homolog family member T1 (RHOT1) in the transfer of mitochondria between oral squamous cell carcinoma cells and macrophages, and to evaluate its impact on tumor cell energy metabolism and malignant behavior. Methods: Macrophages expressing a mitochondria-targeted fluorescent reporter and carcinoma cells with RHOT1 gene knockdown were established. Mitochondrial transfer was quantified using flow cytometry and confocal microscopy. Intracellular energy content, cell proliferation activity, and migratory capacity were assessed through biochemical assays and wound-healing analysis. Results: Knockdown of RHOT1 markedly reduced the ability of carcinoma cells to acquire mitochondria from macrophages. Exogenous mitochondria enhanced the proliferative activity and migratory capacity of negative control cells, whereas no such enhancement was observed in RHOT1-deficient cells. Conclusion: RHOT1 regulates the uptake of macrophage-derived mitochondria by carcinoma cells and thereby influences their energy metabolism and malignant behavior. RHOT1 may serve as a potential target for modulating tumor metabolic adaptation and interactions within the immune microenvironment.

Key words: Ras homolog family member T1, mitochondrial transfer, oral squamous cell carcinoma, macrophage, energy metabolism