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Tumor Biology

, Volume 37, Issue 11, pp 14999–15005 | Cite as

Gamma-synuclein binds to AKT and promotes cancer cell survival and proliferation

  • Zengxia Ma
  • Jianyi Niu
  • Erlian Sun
  • Xuedong Rong
  • Xianxin Zhang
  • Yuanrong Ju
Original Article
  • 147 Downloads

Abstract

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 γ-synuclein, a member of the synuclein family of proteins, on the activation of AKT. We show that the expression level of γ-synuclein is increased in non-small cell lung cancer (NSCLC) tissues. γ-Synuclein binds to the protein kinase domain of AKT and promotes its phosphorylation. Overexpression of γ-synuclein in H157 cells enhances cell proliferation and protects the cells from staurosporine-induced cytotoxicity. Knockdown of γ-synuclein attenuates AKT activation and cell proliferation induced by epidermal growth factor. The effect of γ-synuclein is abolished when AKT is depleted. Thus, γ-synuclein promotes cell survival and proliferation via activating AKT and may play a causal role in the pathogenesis of NSCLC.

Keywords

γ-Synuclein Non-small cell lung cancer H157 cells AKT 

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Copyright information

© International Society of Oncology and BioMarkers (ISOBM) 2016

Authors and Affiliations

  • Zengxia Ma
    • 1
    • 2
  • Jianyi Niu
    • 3
  • Erlian Sun
    • 1
  • Xuedong Rong
    • 2
  • Xianxin Zhang
    • 2
  • Yuanrong Ju
    • 1
  1. 1.Department of RespiratoryShandong Provincial Hospital Affiliated to Shandong UniversityJinanChina
  2. 2.Department of RespiratoryShandong Provincial Chest HospitalJinanChina
  3. 3.Department of Neurology, Yidu Central HospitalWeifang Medical UniversityQingzhouChina

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