The PI3K/AKT/mTOR signaling pathway inhibitors enhance radiosensitivity in cancer cell lines.

Autor: Mardanshahi A; Department of Radiology and Nuclear Medicine, Faculty of Medicine, Cardiovascular Research Center, Mazandaran University of Medical Sciences, Sari, Iran., Gharibkandi NA; Department of Radiopharmacy, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran., Vaseghi S; Department of Chemistry, Science and Research Branch, Islamic Azad University, Tehran, Iran., Abedi SM; Department of Radiology and Nuclear Medicine, Faculty of Medicine, Cardiovascular Research Center, Mazandaran University of Medical Sciences, Sari, Iran., Molavipordanjani S; Department of Radiology and Nuclear Medicine, Faculty of Medicine, Cardiovascular Research Center, Mazandaran University of Medical Sciences, Sari, Iran. sajjad.molavi@gmail.com.
Jazyk: angličtina
Zdroj: Molecular biology reports [Mol Biol Rep] 2021 Aug; Vol. 48 (8), pp. 1-14. Date of Electronic Publication: 2021 Aug 06.
DOI: 10.1007/s11033-021-06607-3
Abstrakt: 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.
(© 2021. The Author(s), under exclusive licence to Springer Nature B.V.)
Databáze: MEDLINE
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