国际口腔医学杂志 ›› 2025, Vol. 52 ›› Issue (2): 246-256.doi: 10.7518/gjkq.2025028

• 综述 • 上一篇    下一篇

磷脂酰肌醇3激酶相关放射抵抗机制在口腔鳞状细胞癌中的研究进展

卢妍蓓1(),李正娟1,雷蕾2(),罗晶晶2   

  1. 1.口腔疾病防治全国重点实验室;国家口腔医学中心 国家口腔疾病临床医学研究中心;口腔医学+前沿医学创新中心 四川大学华西口腔医学院 成都 610041
    2.口腔疾病防治全国重点实验室;国家口腔医学中心 国家口腔疾病临床医学研究中心;口腔医学+前沿医学创新中心 四川大学华西口腔医院预防口腔科 成都 610041
  • 收稿日期:2024-06-04 修回日期:2024-12-07 出版日期:2025-03-01 发布日期:2025-03-01
  • 通讯作者: 雷蕾
  • 作者简介:卢妍蓓,学士,Email:lu_yanbei@163.com
  • 基金资助:
    国家自然科学基金(82001061);四川省自然科学基金(2022NSFSC1377);四川大学华西口腔医学院(华西口腔医院)科研经费资助项目(RCDWJS2024-9)

Research progress on phosphatidylinositol 3-kinase-mediated radioresistance in oral squamous cell carcinoma

Yanbei Lu1(),Zhengjuan Li1,Lei Lei2(),Jingjing Luo2   

  1. 1.State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases & Frontier Innovation Center for Dental Medicine Plus & West China School of Stomatology, Sichuan University, Chengdu 610041, China
    2.State Key Laboratory of Oral Diseases & National Center for Stomatology & Natio-nal Clinical Research Center for Oral Diseases & Frontier Innovation Center for Dental Medicine Plus & Dept. of Preventive Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China
  • Received:2024-06-04 Revised:2024-12-07 Online:2025-03-01 Published:2025-03-01
  • Contact: Lei Lei
  • Supported by:
    National Natural Science Foundation of China(82001061);Sichuan Natural Science Foundation(2022NSFSC1377);Research Funding from West China School/Hospital of Stomatology, Sichuan University(RCDWJS2024-9)

摘要:

口腔鳞状细胞癌(OSCC)是口腔颌面部最常见的恶性肿瘤,恶性程度较高。放射治疗是OSCC综合序列治疗的重要手段,对原位肿瘤治疗效果良好,但术后肿瘤复发和转移较常见,致死率高;其主要原因在于部分肿瘤具有显著的放射抵抗,存活的癌细胞可表现出增殖、侵袭和迁移增强,发生上皮-间充质转化,甚至获得癌干细胞表型。磷脂酰肌醇3激酶/蛋白激酶B(PI3K/PKB,通常称PI3K/Akt)信号通路及其信号组分广泛参与OSCC发生发展和治疗预后的调控,已被证明与OSCC放射抵抗呈正相关;但其具体调控机制仍待进一步探索。本综述聚焦PI3K信号通路与OSCC的放射抵抗,从癌细胞、癌干细胞和肿瘤微环境三方面总结当前的研究进展,讨论PI3K介导的放射抵抗分子机制,以期为提高OSCC放疗敏感性和改善患者预后提供有效的潜在分子靶标。

关键词: 口腔鳞状细胞癌, 放射疗法, 辐射耐受性, 磷脂酰肌醇3激酶

Abstract:

Oral squamous cell carcinoma (OSCC) is the most common type of malignant tumors in craniofacial region with a high malignancy. Radiotherapy, a vital means of integrated sequential therapy for OSCC, often has good treating efficacy for primary tumor. However, it still remains susceptible to the incidence of tumor recurrence and metastasis with high mortality post-radiotherapy. The main reason lies in the significant radioresistance of partial OSCC. The cancer cells survived from Radiotherapy are able to obtain enhanced proliferation, invasion and migration, occur epithelial-mesenchymal transformation, and even acquire cancer stem cell phenotype. Phosphatidylinositol 3-kinase/protein kinase B (PI3K/PKB, often known as PI3K/Akt) signaling pathway and its signaling components widely engaged in regulating the development and prognosis of OSCC, has been reported to promote radioresistance of OSCC when activated. However, the specific mechanism still needs further identification. This review focuses on the mechanism of PI3K signaling and radioresistance in OSCC, and summarize the current research progress from three aspects including cancer cell, cancer stem cell and tumor microenvironment, to discuss the molecular mechanism of PI3K-mediated radioresistance, hoping to provide effective potential molecular target for better radiosensitivity and prognosis of OSCC.

Key words: oral squamous cell carcinoma, radiotherapy, radioresistance, phosphatidylinositol 3-kinase

中图分类号: 

  • R739.8

图 1

PI3K信号通路介导的OSCC放射抵抗机制PDK-1:磷酸肌醇依赖性蛋白激酶-1(3-Phosphoinositide-dependent protein kinase 1)。"

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