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