口腔医学研究 ›› 2026, Vol. 42 ›› Issue (4): 269-273.DOI: 10.13701/j.cnki.kqyxyj.2026.04.001

• 综述 •    下一篇

口腔鳞状细胞癌代谢重编程与蛋白质翻译后修饰的特征及交互调控

尹西腾, 韩伟*   

  1. 南京大学医学院附属口腔医院,南京市口腔医院口腔颌面外科,南京大学口腔医学研究所 江苏 南京 210008
  • 收稿日期:2025-06-18 发布日期:2026-04-23
  • 通讯作者: *韩伟,E-mail: doctorhanwei@hotmail.com
  • 作者简介:尹西腾(1992~ ),男,江苏东海人,主治医师,博士在读,研究方向:肿瘤微环境。
  • 基金资助:
    国家自然科学基金面上项目(编号:82473178) 南京市卫生科技发展专项资金(编号:YKK24199)

Characteristics and Interactive Regulation of Metabolic Reprogramming and Protein Post-translational Modifications in Oral Squamous Cell Carcinoma

YIN Xiteng, HAN Wei*   

  1. Department of Oral and Maxillofacial Surgery, Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing 210008, China
  • Received:2025-06-18 Published:2026-04-23

摘要: 口腔鳞状细胞癌(oral squamous cell carcinoma, OSCC)是头颈部最常见的恶性肿瘤,其高复发转移率亟待发掘新治疗靶点。代谢重编程与蛋白质翻译后修饰(post-translational modification, PTM)作为肿瘤核心特征,在OSCC进展中发挥关键交互作用。OSCC表现出显著的代谢重塑特征,包括糖酵解增强、三羧酸循环与氧化磷酸化动态调整、氨基酸代谢异常及脂质合成亢进等,为癌细胞持续提供能量与生物合成原料。代谢中间产物可充当PTM的底物或辅因子,直接调控表观遗传重编程;而PTM则通过磷酸化、泛素化等修饰动态调节代谢酶活性与通量,实现对代谢通路的反馈调控。这种双向交互网络协同驱动OSCC的恶性进展。本文系统综述了上述机制,旨在为OSCC的分子分型与靶向治疗策略提供理论依据。

关键词: 口腔鳞状细胞癌, 代谢重编程, 蛋白质翻译后修饰, 交互调控

Abstract: Oral squamous cell carcinoma (OSCC), the most prevalent malignant tumor of the head and neck, exhibits high rates of recurrence and metastasis, necessitating novel therapeutic targets. Metabolic reprogramming and post-translational modifications (PTMs), recognized as core hallmarks of cancer, play a critical interactive role in OSCC progression. OSCC demonstrates significant metabolic remodeling features: enhanced glycolysis, dynamic remodeling of the tricarboxylic acid (TCA) cycle and oxidative phosphorylation, dysregulated amino acid metabolism, and hyperactive lipid synthesis, supplying energy and biosynthetic precursors for cancer cells. Metabolic intermediates can serve as substrates or cofactors for PTMs, directly regulating epigenetic reprogramming. Conversely, PTMs dynamically modulate the activity and flux of metabolic enzymes through mechanisms such as phosphorylation and ubiquitination, enabling feedback regulation of metabolic pathways. This bidirectional crosstalk synergistically drives the malignant progression of OSCC. This review summarizes these mechanisms, aiming to provide novel theoretical foundations for molecular subtyping and targeted therapeutic strategies in OSCC.

Key words: oral squamous cell carcinoma, metabolic reprogramming, post-translational modifications, interactive regulation