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

Zengxia Ma1,2, Jianyi Niu3, Erlian Sun1

  • 1Department of Respiratory, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, 250021, China.

Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine
|September 23, 2016
PubMed

Insights

Gamma-synuclein enhances cancer cell survival and proliferation by activating AKT (Protein Kinase B). This protein may play a key role in non-small cell lung cancer development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Hyperactivation of AKT (Protein Kinase B) is crucial for cancer cell survival and proliferation.
  • The precise molecular mechanisms driving AKT activation are not fully understood.
  • Synuclein family proteins, including gamma-synuclein, are implicated in various cellular processes.

Purpose of the Study:

  • To investigate the role of gamma-synuclein in the activation of AKT.
  • To determine the impact of gamma-synuclein on cancer cell behavior, specifically in non-small cell lung cancer (NSCLC).

Main Methods:

  • Quantitative analysis of gamma-synuclein expression in NSCLC tissues.
  • In vitro assays to assess the binding of gamma-synuclein to AKT.
  • Western blot analysis to detect AKT phosphorylation.
  • Cell culture experiments involving overexpression and knockdown of gamma-synuclein in NSCLC cell lines (H157).
  • Assessment of cell proliferation and cytotoxicity assays (staurosporine-induced).
  • Epidermal growth factor (EGF) stimulation experiments.
  • AKT depletion experiments.

Main Results:

  • Gamma-synuclein expression is elevated in NSCLC tissues.
  • Gamma-synuclein directly binds to the protein kinase domain of AKT, promoting its phosphorylation.
  • Overexpression of gamma-synuclein in H157 cells increased cell proliferation and resistance to apoptosis.
  • Knockdown of gamma-synuclein reduced AKT activation and EGF-induced cell proliferation.
  • The effects of gamma-synuclein on AKT activation and cell proliferation were dependent on the presence of AKT.

Conclusions:

  • Gamma-synuclein promotes cancer cell survival and proliferation through the activation of AKT.
  • Gamma-synuclein may contribute causally to the pathogenesis of non-small cell lung cancer.
  • Targeting gamma-synuclein could represent a potential therapeutic strategy for NSCLC.
Keywords:
AKTH157 cellsNon-small cell lung cancerγ-Synuclein

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