Zeng Xiaoli, Chen Yue, Wang Jing, He Miao, Qiu Junyao, Huang Yun
Department of Oncology, The First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi, China.
Jiangxi "Flagship" Oncology Department of Synergy for Chinese and Western Medicine, The First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi, China.
Front Immunol. 2025 Jan 7;15:1535649. doi: 10.3389/fimmu.2024.1535649. eCollection 2024.
Oral cancer is a highly malignant disease characterized by recurrence, metastasis, and poor prognosis. Autophagy, a catabolic process induced under stress conditions, has been shown to play a dual role in oral cancer development and therapy. Recent studies have identified that autophagy activation in oral epithelial cells suppresses cancer cell survival by inhibiting key pathways such as the mammalian target of rapamycin (mTOR) and mitogen-activated protein kinase (MAPK), while activating the adenosine monophosphate-activated protein kinase (AMPK) pathway. Inducing autophagy promotes degradation of eukaryotic initiation factor 4E, thus reducing metastasis and enhancing the efficacy of chemotherapy, radiotherapy, and immunotherapy. Furthermore, autophagy induction can modulate the tumor immune microenvironment and enhance antitumor immunity. This review comprehensively summarizes the relationship between autophagy and oral cancer, focusing on its mechanisms and therapeutic potential when combined with conventional treatments. While promising, the precise mechanisms and clinical applications of autophagy inducers in oral cancer therapy remain to be elucidated, offering new directions for future research to improve treatment outcomes and reduce recurrence.
口腔癌是一种高度恶性的疾病，其特征为复发、转移和预后不良。自噬是在应激条件下诱导产生的一种分解代谢过程，已被证明在口腔癌的发生发展和治疗中发挥双重作用。最近的研究发现，口腔上皮细胞中的自噬激活通过抑制关键通路，如雷帕霉素靶蛋白（mTOR）和丝裂原活化蛋白激酶（MAPK），来抑制癌细胞存活，同时激活腺苷单磷酸活化蛋白激酶（AMPK）通路。诱导自噬可促进真核起始因子4E的降解，从而减少转移并增强化疗、放疗和免疫治疗的疗效。此外，自噬诱导可调节肿瘤免疫微环境并增强抗肿瘤免疫力。本综述全面总结了自噬与口腔癌之间的关系，重点关注其机制以及与传统治疗联合时的治疗潜力。尽管前景广阔，但自噬诱导剂在口腔癌治疗中的精确机制和临床应用仍有待阐明，这为未来研究改善治疗效果和减少复发提供了新方向。
