Immunosurveillance, interferon, and autophagic networking in cancer: the PRKCI-ULK2 paradigm

Autophagy. 2022 Jan;18(1):226-227. doi: 10.1080/15548627.2021.1991192. Epub 2021 Dec 12.

Abstract

The mechanisms controlling immunosurveillance and immunoevasion often operate simultaneously to the triggering of the oncogenic signaling that results in tumor initiation. The resolution of the balance between anti-cancer immune responses and pro-tumorigenic pathways determines if a tumor cell survives and can remodel the microenvironment to reinforce immunosuppression or is eliminated by the immune system. Cancer cells must endure a toxic and metabolically challenging milieu. In its various forms, autophagy provides a way for transformed cells to survive by promoting catabolism and detoxification. Mounting evidence suggests that the boundaries between cancer immunity and mitogenic and metabolic programs are diffuse, with the same molecules likely serving several diverse roles in immunity and metabolism during tumor initiation and progression. Our recent data provide mechanistic detail and functional relevance of a new paradigm whereby the same signaling elements control immunity and autophagy in cancer.

Keywords: Atypical PKC; ULK2; autophagy; immunosurveillance; interferon.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Autophagy / physiology
  • Carcinogenesis
  • Cell Transformation, Neoplastic
  • Humans
  • Interferons*
  • Isoenzymes / metabolism
  • Monitoring, Immunologic
  • Neoplasms* / metabolism
  • Protein Kinase C / metabolism
  • Protein Serine-Threonine Kinases
  • Signal Transduction
  • Tumor Microenvironment

Substances

  • Isoenzymes
  • Interferons
  • Protein Serine-Threonine Kinases
  • Ulk2 protein, human
  • Protein Kinase C
  • protein kinase C lambda