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PPARδ is a regulator of autophagy by its phosphorylation

Qian Gou1, Yidan Jiang1, Runyun Zhang1

  • 1Institute of Life Science, Jiangsu University, Zhenjiang, Jiangsu Province, 212013, People's Republic of China.

Oncogene
|May 23, 2020
PubMed

Insights

Epidermal Growth Factor Receptor (EGFR) activation suppresses autophagy by phosphorylating PPARδ, inhibiting nutrient recycling and promoting tumor growth. This phosphorylation links EGFR signaling to autophagy regulation.

Area of Science:

  • Cellular Biology
  • Molecular Oncology
  • Autophagy Research

Background:

  • Autophagy is a cellular process for nutrient recycling, suppressed by growth factors like EGFR.
  • The role of PPARδ in EGFR-mediated autophagy regulation was previously unknown.

Purpose of the Study:

  • To investigate if PPARδ regulates autophagy in response to active EGFR.
  • To elucidate the mechanism of EGFR-mediated autophagy suppression.

Main Methods:

  • Investigated EGFR-induced PPARδ phosphorylation at tyrosine-108.
  • Analyzed the interaction between LC3 and PPARδ using its LIR motif.
  • Assessed the impact of EGFR activation and inhibition on autophagic flux and tumor growth.

Main Results:

  • EGFR induces PPARδ phosphorylation at tyrosine-108.
  • Phosphorylated PPARδ binds to LC3, inhibiting autophagic flux.
  • EGFR inhibitor treatment reversed these effects.
  • EGFR-mediated PPARδ phosphorylation correlated with autophagy inhibition and tumor growth.

Conclusions:

  • PPARδ acts as a key regulator of autophagy.
  • EGFR signaling suppresses autophagy through PPARδ phosphorylation.
  • This pathway is implicated in tumor growth.

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