PKCλ/ι Loss Induces Metabolic Reprogramming in Liver Cancer: Hitting Two Birds with One Stone?

Pierluigi Ramadori; Xin Li; Mathias Heikenwalder

doi:10.1016/j.ccell.2020.07.003

PKCλ/ι Loss Induces Metabolic Reprogramming in Liver Cancer: Hitting Two Birds with One Stone?

Cancer Cell. 2020 Aug 10;38(2):152-154. doi: 10.1016/j.ccell.2020.07.003.

Authors

Pierluigi Ramadori¹, Xin Li², Mathias Heikenwalder³

Affiliations

¹ Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ) Heidelberg, 69120 Heidelberg, Germany. Electronic address: [email protected].
² Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ) Heidelberg, 69120 Heidelberg, Germany.
³ Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ) Heidelberg, 69120 Heidelberg, Germany. Electronic address: [email protected].

PMID: 32781040
DOI: 10.1016/j.ccell.2020.07.003

Abstract

In this issue of Cancer Cell, Kudo et al. identify a novel tumor suppressor role for PKCλ/ι in hepatocellular carcinoma. Loss of PKCλ/ι in obesity-driven liver cancer results in cellular metabolic reprogramming that induces two reciprocally sustainable processes, oxidative phosphorylation and autophagy, which promote liver-tumor aggressiveness in an NRF2-dependent manner.

Publication types

Research Support, Non-U.S. Gov't
Comment

MeSH terms

Autophagy
Humans
Isoenzymes / metabolism
Liver Neoplasms*
NF-E2-Related Factor 2
Oxidative Phosphorylation*
Protein Kinase C / metabolism

Substances

Isoenzymes
NF-E2-Related Factor 2
Protein Kinase C