共 91 条
ATM: Main Features, Signaling Pathways, and Its Diverse Roles in DNA Damage Response, Tumor Suppression, and Cancer Development
被引:61
作者:

Phan, Liem Minh
论文数: 0 引用数: 0
h-index: 0
机构:
Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, 1515 Holcombe Blvd, Houston, TX 77030 USA Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, 1515 Holcombe Blvd, Houston, TX 77030 USA

Rezaeian, Abdol-Hossein
论文数: 0 引用数: 0
h-index: 0
机构:
Univ South Carolina, Coll Pharm, Dept Drug Discovery & Biomed Sci, Columbia, SC 29208 USA Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, 1515 Holcombe Blvd, Houston, TX 77030 USA
机构:
[1] Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, 1515 Holcombe Blvd, Houston, TX 77030 USA
[2] Univ South Carolina, Coll Pharm, Dept Drug Discovery & Biomed Sci, Columbia, SC 29208 USA
来源:
关键词:
ATM;
cancer;
DNA damage repair;
DNA damage response;
oxidative sensing;
autophagy;
hypoxia;
pexophagy;
mitophagy;
cellular homeostasis;
DOUBLE-STRAND BREAKS;
ATAXIA-TELANGIECTASIA GENE;
OXIDATIVE STRESS;
PROTEIN-KINASE;
ACTIVATION;
REPAIR;
PHOSPHORYLATION;
TRANSCRIPTION;
AUTOPHAGY;
TARGET;
D O I:
10.3390/genes12060845
中图分类号:
Q3 [遗传学];
学科分类号:
071007 ;
090102 ;
摘要:
ATM is among of the most critical initiators and coordinators of the DNA-damage response. ATM canonical and non-canonical signaling pathways involve hundreds of downstream targets that control many important cellular processes such as DNA damage repair, apoptosis, cell cycle arrest, metabolism, proliferation, oxidative sensing, among others. Of note, ATM is often considered a major tumor suppressor because of its ability to induce apoptosis and cell cycle arrest. However, in some advanced stage tumor cells, ATM signaling is increased and confers remarkable advantages for cancer cell survival, resistance to radiation and chemotherapy, biosynthesis, proliferation, and metastasis. This review focuses on addressing major characteristics, signaling pathways and especially the diverse roles of ATM in cellular homeostasis and cancer development.
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