Alireza Mardanshahi1, Nasrin Abbasi Gharibkandi2, Samaneh Vaseghi3, Seyed Mohammad Abedi1, Sajjad Molavipordanjani4. 1. Department of Radiology and Nuclear Medicine, Faculty of Medicine, Cardiovascular Research Center, Mazandaran University of Medical Sciences, Sari, Iran. 2. Department of Radiopharmacy, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran. 3. Department of Chemistry, Science and Research Branch, Islamic Azad University, Tehran, Iran. 4. Department of Radiology and Nuclear Medicine, Faculty of Medicine, Cardiovascular Research Center, Mazandaran University of Medical Sciences, Sari, Iran. sajjad.molavi@gmail.com.
Abstract
INTRODUCTION: Radiotherapy is one of the most common types of cancer treatment modalities. Radiation can affect both cancer and normal tissues, which limits the whole delivered dose. It is well documented that radiation activates phosphatidylinositol 3-kinase (PI3K) and AKT signaling pathway; hence, the inhibition of this pathway enhances the radiosensitivity of tumor cells. The mammalian target of rapamycin (mTOR) is a regulator that is involved in autophagy, cell growth, proliferation, and survival. CONCLUSION: The inhibition of mTOR as a downstream mediator of the PI3K/AKT signaling pathway represents a vital option for more effective cancer treatments. The combination of PI3K/AKT/mTOR inhibitors with radiation can increase the radiosensitivity of malignant cells to radiation by autophagy activation. Therefore, this review aims to discuss the impact of such inhibitors on the cell response to radiation.
INTRODUCTION: Radiotherapy is one of the most common types of cancer treatment modalities. Radiation can affect both cancer and normal tissues, which limits the whole delivered dose. It is well documented that radiation activates phosphatidylinositol 3-kinase (PI3K) and AKT signaling pathway; hence, the inhibition of this pathway enhances the radiosensitivity of tumor cells. The mammalian target of rapamycin (mTOR) is a regulator that is involved in autophagy, cell growth, proliferation, and survival. CONCLUSION: The inhibition of mTOR as a downstream mediator of the PI3K/AKT signaling pathway represents a vital option for more effective cancer treatments. The combination of PI3K/AKT/mTOR inhibitors with radiation can increase the radiosensitivity of malignant cells to radiation by autophagy activation. Therefore, this review aims to discuss the impact of such inhibitors on the cell response to radiation.