期刊
CELL CYCLE
卷 20, 期 8, 页码 742-751出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2021.1897271
关键词
mTOR; DNA replication origin licensing; replication fork progression; replication fork stabilization; cell cycle; DNA repair
类别
资金
- American Cancer Society [IRG-67-003-47]
- National Institute of Health [R01CA246553]
- Major Research Project of Science Technology Department of Zhejiang Province [2021C03124]
- Wu Jieping Medical Foundation [320.6750.19092-12]
Accurate and complete DNA replication and separation are crucial for genetic information inheritance and organism maintenance. Errors in DNA duplication are the main source of genetic instability and understanding DNA duplication regulation is essential for elucidating mechanisms and finding treatment strategies for human genetic disorders, especially cancer. The mechanistic target of rapamycin (mTOR) plays a central role in cell growth and proliferation by monitoring cell physiology, and its dysregulation is associated with various human diseases, including cancer and diabetes. Emerging evidence suggests that mTOR signaling is key in regulating DNA replication, including origin licensing, replication fork progression, and stabilization.
Accurate and complete DNA replication and separation are essential for genetic information inheritance and organism maintenance. Errors in DNA duplication are the main source of genetic instability. Understanding DNA duplication regulation is the key to elucidate the mechanisms and find treatment strategies for human genetic disorders, especially cancer. The mechanistic target of rapamycin (mTOR) is a central regulator of cell growth and proliferation by integrating and processing extracellular and intracellular signals to monitor the well-being of cell physiology. mTOR signaling dysregulation is associated with many human diseases including cancer and diabetes. Emerging evidence has demonstrated that mTOR signaling plays a key role in DNA duplication. We herein review the current knowledge of mTOR signaling in the regulation of DNA replication origin licensing, replication fork progression, and stabilization.
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