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PIASy antagonizes Ras-driven NSCLC survival by promoting GATA2 SUMOylation

Bin Chen1,2, Jie Luo1, Yirui Zhou1

  • 1Department of Oncology, Shanghai Pulmonary Hospital, Shanghai Tongji University, Shanghai 200433, China.

Journal of Cancer
|May 16, 2018
PubMed

Insights

Protein inhibitor of activated STAT y (PIASy) suppresses RAS-driven non-small cell lung cancer (NSCLC) by enhancing GATA2 SUMOylation. Decreased PIASy expression correlates with RAS mutations, suggesting PIASy as a therapeutic target in NSCLC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The GATA2 transcriptional network is crucial for RAS oncogene-driven non-small cell lung cancer (NSCLC).
  • GATA2 is a SUMOylated protein, and its activity is modulated by SUMO-2 conjugation catalyzed by PIASy in endothelial cells.

Purpose of the Study:

  • To investigate the role of PIASy in RAS-mutant NSCLC.
  • To determine the mechanism by which PIASy affects GATA2 activity in NSCLC.

Main Methods:

  • Analysis of PIASy expression in NSCLC cell lines and patient specimens with RAS mutations.
  • Forced expression of PIASy in NSCLC cells to assess its effect on cell viability, tumorigenesis, and growth.
  • Investigation of GATA2 transcriptional network alterations and GATA2 SUMOylation levels upon PIASy overexpression.

Main Results:

  • PIASy expression was decreased in RAS-mutant NSCLC.
  • Forced PIASy expression inhibited NSCLC cell viability, tumorigenesis, and growth in vitro and in vivo.
  • PIASy overexpression altered GATA2-regulated pathways (proteasome, IL-1, Rho signaling) and increased GATA2 SUMOylation, reducing its transcriptional activity.

Conclusions:

  • PIASy acts as an antagonist in RAS-driven NSCLC.
  • PIASy suppresses NSCLC by enhancing GATA2 SUMOylation and inhibiting its transcriptional activity.
  • PIASy represents a potential therapeutic target for RAS-driven NSCLC.
Keywords:
GATA2NSCLCPIASyRasSUMOylaition

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