PI3K/AKT/mTOR signaling in gastric cancer: Epigenetics and beyond

被引:261
作者
Fattahi, Sadegh [1 ,2 ,3 ]
Amjadi-Moheb, Fatemeh [4 ]
Tabaripour, Reza [5 ]
Ashrafi, Gholam Hossein [6 ]
Akhavan-Niaki, Haleh [4 ]
机构
[1] Babol Univ Med Sci, Student Res Comm, Babol, Iran
[2] Babol Univ Med Sci, Hlth Res Inst, Cellular & Mol Biol Res Ctr, Babol, Iran
[3] Pasteur Inst, North Res Ctr, Amol, Iran
[4] Babol Univ Med Sci, Dept Genet, Fac Med, Babol, Iran
[5] Islamic Azad Univ, Dept Cellular & Mol Biol, Babol Branch, Babol, Iran
[6] Kingston Univ London, Sch Life Sci Pharm & Chem, SEC Fac, Canc Theme, London KT12EE, England
关键词
PI3K/AKT/mTOR pathway; Epigenetic modulation; Gastric cancer; Chemoresistance; Non-coding RNAs; Targeted therapy; PROMOTES CISPLATIN RESISTANCE; INHIBITS CELL-PROLIFERATION; ABERRANT DNA METHYLATION; HUMAN OVARIAN-CANCER; NF-KAPPA-B; AKT INHIBITOR; UP-REGULATION; PHOSPHOINOSITIDE; 3-KINASES; MESENCHYMAL TRANSITION; SCAFFOLDING FUNCTION;
D O I
10.1016/j.lfs.2020.118513
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
PI3K/AKT/mTOR pathway is one of the most important signaling pathways involved in normal cellular processes. Its aberrant activation modulates autophagy, epithelial-mesenchymal transition, apoptosis, chemoresistance, and metastasis in many human cancers. Emerging evidence demonstrates that some infections as well as epigenetic regulatory mechanisms can control PI3K/AKT/mTOR signaling pathway. In this review, we focused on the role of this pathway in gastric cancer development, prognosis, and metastasis, with an emphasis on epigenetic alterations including DNA methylation, histone modifications, and post-transcriptional modulations through non-coding RNAs fluctuations as well as H. pylori and Epstein-Barr virus infections. Finally, we reviewed different molecular targets and therapeutic agents in clinical trials as a potential strategy for gastric cancer treatment through the PI3K/AKT/mTOR pathway.
引用
收藏
页数:16
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