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Protein kinase Cλ/ι in cancer: a contextual balance of time and signals

Jorge Moscat1, Juan F Linares1, Angeles Duran1

  • 1Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, 1300 York Avenue, New York, NY 10065, USA.

Trends in Cell Biology
|May 2, 2022
PubMed

Insights

Protein kinase Cλ/ι (PKCλ/ι) normally suppresses cancer by blocking metabolic pathways. Its reduction can drive tumorigenesis, but inflammation and other signals modulate this effect, impacting cancer development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Non-oncogenic drivers influence cancer vulnerabilities.
  • Protein kinase Cλ/ι (PKCλ/ι) inhibits tumorigenesis by regulating metabolism and epigenetic control.
  • PKCλ/ι loss activates metabolic pathways but also triggers anti-tumor immunity via the STING pathway.

Purpose of the Study:

  • To review the molecular and cellular functions of PKCλ/ι in cancer.
  • To explore the interplay between metabolism and inflammation in the tumor microenvironment.
  • To elucidate how PKCλ/ι influences tumorigenesis in different signaling contexts.

Main Methods:

  • Literature review of molecular and cellular mechanisms.
  • Analysis of signaling pathways including WNT/β-catenin and PKCζ.
  • Examination of the tumor microenvironment's metabolic and inflammatory crosstalk.

Main Results:

  • PKCλ/ι acts as a tumor suppressor by controlling metabolic fuel oxidation.
  • Reduced PKCλ/ι unleashes metabolic pathways, potentially promoting cancer.
  • The STING-interferon pathway activated by PKCλ/ι loss can prevent tumor initiation.
  • Context-dependent signaling (WNT/β-catenin, PKCζ) and timing influence whether PKCλ/ι deletion promotes or inhibits cancer.

Conclusions:

  • PKCλ/ι plays a dual role in cancer, acting as a context-dependent regulator.
  • Metabolic reprogramming and immune surveillance are critical in PKCλ/ι-mediated tumor suppression.
  • Understanding the crosstalk between metabolism and inflammation is key to targeting PKCλ/ι in cancer therapy.
Keywords:
autophagycancerinterferonmetabolismprotein kinase Ctumor microenvironment

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