口腔医学 ›› 2026, Vol. 46 ›› Issue (8): 624-628.doi: 10.13591/j.cnki.kqyx.2026.08.010

• 综述 • 上一篇    下一篇

EP300在口腔鳞状细胞癌中的核心角色:调控机制与临床前景

张超, 韩莉, 刘家宏, 毛周洪, 付浩轩, 唐婉容()   

  1. 川北医学院口腔医学院, 四川南充 (637000)
  • 收稿日期:2025-09-25 出版日期:2026-08-28 发布日期:2026-08-21
  • 通讯作者: 唐婉容 E-mail:642533674@qq.com
  • 基金资助:
    川北医学院科研发展计划(CBY23-ZDA10)

The central role of EP300 in oral squamous cell carcinoma: Regulatory mechanisms and clinical prospects

ZHANG Chao, HAN Li, LIU Jiahong, MAO Zhouhong, FU Haoxuan, TANG Wanrong()   

  1. School of Stomatology, North Sichuan Medical College, Nanchong 637000, China
  • Received:2025-09-25 Online:2026-08-28 Published:2026-08-21

摘要:

口腔鳞状细胞癌(oral squamous cell carcinoma, OSCC)是头颈部最为常见的恶性肿瘤,其发生发展涉及多步骤、多基因参与的复杂生物学过程。在这一过程中,表观遗传学调控,尤其是组蛋白修饰,发挥着关键作用。EP300作为一种重要的转录辅激活因子,具有内在组蛋白乙酰转移酶(histone acetyltransferase, HAT)活性,能够通过乙酰化修饰组蛋白及多种非组蛋白,广泛参与染色质结构重塑、基因转录调控、细胞周期进程、DNA损伤修复、细胞分化与凋亡等重要生命活动。近年研究表明,EP300在OSCC中表现出功能上的双重性与复杂性:其功能失调可影响肿瘤的恶性进展;而在某些情境下,其过表达亦可能通过激活不同的致癌信号通路,进而驱动肿瘤生长。本文旨在系统梳理EP300在OSCC中的表达特征、调控机制,并重点阐述其通过与p53、Wnt/β-catenin、Notch、NF-κB等关键信号通路相互作用,参与OSCC发生发展的分子基础。此外,本文还将探讨以EP300及其相关通路为靶点的新型治疗策略在OSCC中的潜力与挑战,并对该领域的未来研究方向作出展望。

关键词: 口腔鳞状细胞癌, EP300, 表观遗传学, 信号通路, 分子靶向治疗

Abstract:

Oral squamous cell carcinoma (OSCC) is the most common malignant tumor of the head and neck region, whose pathogenesis involves a complex, multi-step process with the participation of multiple genes. Epigenetic regulation, particularly histone modifications, plays a critical role in this process. EP300 is a key transcriptional coactivator with intrinsic histone acetyltransferase (HAT) activity. It mediates the acetylation of both histone and non-histone proteins, thereby widely participating in essential biological processes such as chromatin remodeling, gene transcription, cell cycle progression, DNA damage repair, cell differentiation, and apoptosis. Recent studies have revealed a dual and complex role of EP300 in OSCC: while its dysfunction can influence tumor progression, its overexpression may, under certain circumstances, drive tumor growth by activating various oncogenic pathways. This review aims to systematically elucidate the expression status and regulatory mechanisms of EP300 in OSCC, and to elaborate on the molecular mechanisms through which it interacts with multiple signaling pathways (such as p53, Wnt/β-catenin, Notch, and NF-κB) to influence the initiation and progression of OSCC. Furthermore, we will discuss the potential and challenges of targeting EP300 and its related pathways as a novel therapeutic strategy for OSCC, and look into the prospect of future research directions.

Key words: oral squamous cell carcinoma, EP300, epigenetics, signaling pathway, molecular targeted therapy

中图分类号: