生物
mTORC1型
P70-S6激酶1
细胞生物学
PI3K/AKT/mTOR通路
翻译(生物学)
蛋白质生物合成
起始因子
信号转导
平动调节
真核起始因子
真核翻译
TOR信号
信使核糖核酸
分子生物学
基因
遗传学
作者
Wei Wang,Zizheng Dong,Yanfei Huang,Jingyuan Liu,Jian‐Ting Zhang
出处
期刊:Oncogene
[Springer Nature]
日期:2022-03-12
卷期号:41 (17): 2431-2443
被引量:13
标识
DOI:10.1038/s41388-022-02262-5
摘要
eIF3a (eukaryotic translation initiation factor 3a), a subunit of the eIF3 complex, has been suggested to play a regulatory role in protein synthesis and in cellular response to DNA-damaging treatments. S6K1 is an effector and a mediator of mTOR complex 1 (mTORC1) in regulating protein synthesis and integrating diverse signals into control of cell growth and response to stress. Here, we show that eIF3a regulates S6K1 activity by inhibiting mTORC1 kinase via regulating Raptor synthesis. The regulation of Raptor synthesis is via eIF3a interaction with HuR (human antigen R) and binding of the eIF3a-HuR complex to the 5'-UTR of Raptor mRNA. Furthermore, mTORC1 may mediate eIF3a function in cellular response to cisplatin by regulating synthesis of NER proteins and NER activity. Taken together, we conclude that the mTOR signaling pathway may also be regulated by translational control and mediate eIF3a regulation of cancer cell response to cisplatin by regulating NER protein synthesis.
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