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Emerging roles of microRNAs in regulating the mTOR signaling pathway during tumorigenesis
被引:12
|作者:
Javid, Hossein
[1
,2
]
Soltani, Arash
[1
,2
]
Mohammadi, Fariba
[1
,2
]
Hashemy, Seyed Isaac
[1
,3
]
机构:
[1] Mashhad Univ Med Sci, Fac Med, Dept Clin Biochem, Mashhad, Razavi Khorasan, Iran
[2] Mashhad Univ Med Sci, Fac Med, Student Res Comm, Mashhad, Razavi Khorasan, Iran
[3] Mashhad Univ Med Sci, Surg Oncol Res Ctr, Mashhad 9177948564, Razavi Khorasan, Iran
关键词:
autophagy;
cancer;
mammalian target of rapamycin;
microRNAs;
phosphoinositide;
3-kinase;
PROMOTES CELL-PROLIFERATION;
HUMAN GASTRIC-CANCER;
DOWN-REGULATION;
MAMMALIAN TARGET;
HEPATOCELLULAR-CARCINOMA;
MIR-144;
SUPPRESSES;
TUMOR-SUPPRESSOR;
GROWTH;
RAPAMYCIN;
INVASION;
D O I:
10.1002/jcb.28401
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
The mammalian target of rapamycin (mTOR) is a large Ser/Thr protein kinase that belongs to the phosphoinositide 3-kinase (PI3K) family and mediates various physiological and pathological processes, especially cell proliferation, protein synthesis, autophagy, and cancer development. The mTOR expression is transient and tightly regulated in normal cells, but it is overactivated in cancer cells. Recently, several studies have indicated that microRNAs (miRNAs) play a critical role in the regulation of mTOR and mTOR-associated processes, some acting as inhibitors and the others as activators. Although it is still in infancy, the strategy of combining both miRNAs and mTOR inhibitors might provide an approach to selectively sensitizing tumor cells to chemotherapy-induced DNA damage and subsequently attenuating the tumor cell growth and apoptosis.
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页码:10874 / 10883
页数:10
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