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mTor is a signaling hub in cell survival: a mass-spectrometry-based proteomics investigation

Zhi Tang1, Ahmet Tarik Baykal, Hui Gao

  • 1KI-Alzheimer Disease Research Center, Karolinska Institutet , SE 14186 Huddinge, Sweden.

Journal of Proteome Research
|April 4, 2014
PubMed

Insights

Mammalian target of rapamycin complex 2 (mTORC2) promotes cell survival by activating pro-survival proteins and inhibiting the mitochondria-caspase-apoptotic pathway. This mTORC2 activity was observed in neuroblastoma cells under serum deprivation.

Area of Science:

  • Cell Biology
  • Neuroscience
  • Molecular Biology

Background:

  • Mammalian target of rapamycin (mTOR) is crucial for protein homeostasis and cell survival.
  • mTOR signaling pathway dysregulation is linked to Alzheimer's disease (AD).
  • mTOR complex 1 (mTORC1) is implicated in the formation of toxic phospho-tau in AD.

Purpose of the Study:

  • To investigate the role of mTOR signaling in cell survival using genetically modified human neuroblastoma SH-SY5Y cells.
  • To identify specific protein expression changes related to cell survival modulated by mTOR activity.
  • To determine the distinct roles of mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2) in cell viability.

Main Methods:

  • Mass-spectrometry-based proteomics to analyze protein expression changes.
  • Flow cytometry to assess cell viability.
  • Genetic modification of mTOR in SH-SY5Y cells.
  • Induction of cell death via moderate serum deprivation.

Main Results:

  • Up-regulated mTOR complex 2 (mTORC2) significantly increased the number of viable cells.
  • Proteomic analysis identified key proteins involved in mitochondrial integrity, apoptosis, and pro-survival functions altered by mTOR modulation.
  • Proteins identified include Thioredoxin-dependent peroxide reductase, Peroxiredoxin-5, Cofilin 1, Annexin A5, Mortalin, and 14-3-3 protein zeta/delta.

Conclusions:

  • mTORC2, not mTORC1, plays a significant role in modulating cell viability.
  • mTORC2 promotes cell survival by activating pro-survival mechanisms and suppressing the mitochondria-caspase-apoptotic pathway.
  • Upregulated mTORC2 may be a key factor in promoting cell survival in vitro.

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