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PI3K/AKT/mTOR 信号通路抑制剂增强癌细胞系的放射敏感性。

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

机构信息

Department of Radiology and Nuclear Medicine, Faculty of Medicine, Cardiovascular Research Center, Mazandaran University of Medical Sciences, Sari, Iran.

Department of Radiopharmacy, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran.

出版信息

Mol Biol Rep. 2021 Aug;48(8):1-14. doi: 10.1007/s11033-021-06607-3. Epub 2021 Aug 6.

DOI:10.1007/s11033-021-06607-3
PMID:34357550
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.

摘要

简介

放射治疗是最常见的癌症治疗方式之一。辐射会影响癌症组织和正常组织,这限制了整个治疗剂量。有充分的文献记载表明,辐射会激活磷脂酰肌醇 3-激酶(PI3K)和 AKT 信号通路;因此,抑制该通路可以提高肿瘤细胞的放射敏感性。雷帕霉素靶蛋白(mTOR)是一种调节因子,参与自噬、细胞生长、增殖和存活。

结论

作为 PI3K/AKT 信号通路的下游介质,mTOR 的抑制代表了更有效癌症治疗的重要选择。PI3K/AKT/mTOR 抑制剂与辐射的联合应用可以通过自噬激活来提高恶性细胞对辐射的放射敏感性。因此,本综述旨在讨论这些抑制剂对细胞对辐射的反应的影响。

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