Int J Stomatol

Int J Stomatol ›› 2025, Vol. 52 ›› Issue (2): 246-256.doi: 10.7518/gjkq.2025028

• Reviews • Previous Articles     Next Articles

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 E-mail:lu_yanbei@163.com;leilei@scu.edu.cn
  • 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)

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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

CLC Number: 

  • R739.8

TrendMD: 

Fig 1

The mechanism of radioresistance in OSCC mediated by PI3K signaling pathway"

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