Protein kinase Cλ/ι in cancer: a contextual balance of time and signals. Review uri icon

Overview

abstract

  • Nononcogenic cancer drivers often impinge on complex signals that create new addictions and vulnerabilities. Protein kinase Cλ/ι (PKCλ/ι) suppresses tumorigenesis by blocking metabolic pathways that regulate fuel oxidation and create building blocks for the epigenetic control of cell differentiation. Reduced levels of PKCλ/ι unleash these pathways to promote tumorigenesis, but the simultaneous activation of the STING-driven interferon cascade prevents tumor initiation by triggering immunosurveillance mechanisms. However, depending on the context of other signaling pathways, such as WNT/β-catenin or PKCζ, and timing, PKCλ/ι deletion can promote or inhibit tumorigenesis. In this review, we discuss in detail the molecular and cellular underpinnings of PKCλ/ι functions in cancer with the perspective of the crosstalk between metabolism and inflammation in the tumor microenvironment.

publication date

  • April 29, 2022

Research

keywords

  • Isoenzymes
  • Neoplasms

Identity

PubMed Central ID

  • PMC9716658

Scopus Document Identifier

  • 85129946127

Digital Object Identifier (DOI)

  • 10.1016/j.tcb.2022.04.002

PubMed ID

  • 35501226

Additional Document Info

volume

  • 32

issue

  • 12