Gamma-synuclein binds to AKT and promotes cancer cell survival and proliferation
作者
作者单位
摘要
Hyperactivation of AKT plays a critical role in the survival and proliferation of cancer cells. However, the molecular mechanisms underlying AKT activation remain elusive. Here, we tested the effect of gamma-synuclein, a member of the synuclein family of proteins, on the activation of AKT. We show that the expression level of gamma-synuclein is increased in non-small cell lung cancer (NSCLC) tissues. gamma-Synuclein binds to the protein kinase domain of AKT and promotes its phosphorylation. Overexpression of gamma-synuclein in H157 cells enhances cell proliferation and protects the cells from staurosporine-induced cytotoxicity. Knockdown of gamma-synuclein attenuates AKT activation and cell proliferation induced by epidermal growth factor. The effect of gamma-synuclein is abolished when AKT is depleted. Thus, gamma-synuclein promotes cell survival and proliferation via activating AKT and may play a causal role in the pathogenesis of NSCLC.
关键词
LUNG-CANCER; MTOR PATHWAY; GENE; KINASE; EXPRESSION; IDENTIFICATION; METASTASIS; RESISTANCE; MUTATION; THERAPY
基本信息
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所属机构:
归属医师: 鞠远荣 孙尔莲
PMID:27655287
UT:000388799900061
刊名:TUMOR BIOLOGY
年,卷(期):2016年37卷11期
页码:14999-15005
DOI:10.1007/s13277-016-5371-9
附件:
收录: SCIE