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A circuit for secretion-coupled cellular autonomy in multicellular eukaryotic cells.

Lingxia Qiao1, Saptarshi Sinha2, Amer Ali Abd El-Hafeez2

  • 1Department of Mechanical and Aerospace Engineering, Jacob's School of Engineering, University of California San Diego, La Jolla, CA, USA.

Molecular Systems Biology
|March 1, 2023
PubMed
Summary

Cancer cells achieve self-sufficient growth by "secreting-and-sensing" growth factors. A novel GTPase circuit, involving Arf1 and Giαβγ, enables this secretion-coupled autonomy, sustaining cell survival.

Keywords:
G proteinsGolgi secretioncellular autonomydose-response alignment (DoRA)epidermal growth factor receptor (EGFR)

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Area of Science:

  • Cell Biology
  • Cancer Biology
  • Molecular Biology

Background:

  • Cancers exhibit autonomous growth signaling, fueled by self-secretion and sensing of growth factors (GFs).
  • The precise mechanisms underlying this "secrete-and-sense" phenomenon remain poorly understood.
  • GIV/Girdin protein links Ras-superfamily GTPases and is implicated in aggressive cancer traits.

Purpose of the Study:

  • To dissect the impact of a feedback-coupled GTPase circuit on secretion-coupled autonomy in cancer cells.
  • To elucidate how Arf1 and Giαβγ GTPases coregulate secretion and sensing.
  • To understand the role of GIV/Girdin in integrating these pathways.

Main Methods:

  • Integrated computational and experimental approaches.
  • Analysis of a feedback-coupled GTPase circuit involving Arf1 and Giαβγ.
  • Proteomic studies and protein-protein interaction network analyses.

Main Results:

  • A circuit with forward and negative feedback loops was identified, enabling closed-loop control between Arf1 and Giαβγ.
  • This circuit converts switch-like secretion into dose-response alignment of sensing and secretion.
  • Stimulus-proportionate secretion sustains cancer cell survival, with GFs like epidermal GF identified as key stimuli.

Conclusions:

  • Enhanced coupling of GTPase switches in cancer cells is critical for multiscale feedback control.
  • This mechanism achieves secretion-coupled autonomy, driving self-sustained growth.
  • Targeting this circuit may offer new therapeutic strategies for aggressive cancers.