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PRKCI negatively regulates autophagy via PIK3CA/AKT-MTOR signaling

Liujing Qu1, Ge Li1, Dan Xia1

  • 1Key Laboratory of Medical Immunology, Ministry of Health, Peking University Health Sciences Center, Beijing, China; Peking University Center for Human Disease Genomics, Peking University, Beijing, China.

Biochemical and Biophysical Research Communications
|January 22, 2016
PubMed

Insights

Protein kinase C iota (PRKCI) impairs autophagy when overexpressed. Reducing PRKCI enhances autophagy, suggesting therapeutic potential for PRKCI-overexpressing cancers.

Area of Science:

  • Cell Biology
  • Molecular Oncology

Background:

  • Atypical protein kinase Ciota (PRKCI) is an oncogene implicated in cell proliferation and differentiation.
  • Dysregulation of autophagy is linked to various diseases, including cancer.

Purpose of the Study:

  • To investigate the role of PRKCI in the regulation of cellular autophagy.
  • To explore the potential of targeting PRKCI for cancer therapy.

Main Methods:

  • Overexpression and knockdown of PRKCI in U2OS cells.
  • Assessment of autophagy markers, including LC3B-II levels and autophagic substrate degradation.
  • Analysis of signaling pathways, specifically PIK3CA/AKT-MTOR.

Main Results:

  • PRKCI overexpression inhibited autophagy, evidenced by decreased LC3B-II and impaired substrate degradation.
  • PRKCI knockdown promoted autophagy.
  • Novel PRKCI mutants (PRKCI(L485M) and PRKCI(P560R)) induced autophagy with dominant-negative effects.
  • PRKCI knockdown-induced autophagy correlated with PIK3CA/AKT-MTOR pathway inactivation.

Conclusions:

  • PRKCI plays a critical role in regulating autophagy.
  • Modulating PRKCI activity offers a potential therapeutic strategy for PRKCI-overexpressing carcinomas with enhanced autophagy.
Keywords:
AutophagyMTORPRKCI

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