2024.04.29 | Peramaiyan Rajendran, Ramya Sekar, Prabhu Shankar Dhayasankar, Enas M Ali, Salaheldin Abdelaouf Abdelsalam, Sabarinath Balaraman, Biju Vadakkemukadiyil Chellappan, Ashraf M. Metwally, Basem M Abdallah
Oral cancer is a highly heterogeneous disease, and the PI3K/AKT/mTOR pathway is a key regulator of cellular and metabolic activities, making it a therapeutic target. This review highlights the role of the PI3K/AKT/mTOR pathway in controlling autophagy and apoptosis during the progression and metastasis of oral squamous cell carcinoma (OSCC). The pathway is activated by various upstream activators and downstream effectors, which can be targeted for therapeutic intervention. The review also discusses the involvement of reactive oxygen species (ROS) in autophagy and the potential of PI3K/AKT/mTOR inhibitors in treating OSCC. Despite the promising results, challenges such as drug resistance and the need for personalized treatments remain. The field of theranostics is crucial for improving the prognosis of OSCC patients, and targeted therapies that modulate the PI3K/AKT/mTOR pathway show promise in this regard.Oral cancer is a highly heterogeneous disease, and the PI3K/AKT/mTOR pathway is a key regulator of cellular and metabolic activities, making it a therapeutic target. This review highlights the role of the PI3K/AKT/mTOR pathway in controlling autophagy and apoptosis during the progression and metastasis of oral squamous cell carcinoma (OSCC). The pathway is activated by various upstream activators and downstream effectors, which can be targeted for therapeutic intervention. The review also discusses the involvement of reactive oxygen species (ROS) in autophagy and the potential of PI3K/AKT/mTOR inhibitors in treating OSCC. Despite the promising results, challenges such as drug resistance and the need for personalized treatments remain. The field of theranostics is crucial for improving the prognosis of OSCC patients, and targeted therapies that modulate the PI3K/AKT/mTOR pathway show promise in this regard.