Mitochondrial metabolic reprogramming: An important player in liver cancer progression

Tianqiang Jin; Chao Wang; Yu Tian; Chaoliu Dai; Yuwen Zhu; Feng Xu

doi:10.1016/j.canlet.2019.11.029

Mitochondrial metabolic reprogramming: An important player in liver cancer progression

Cancer Lett. 2020 Feb 1:470:197-203. doi: 10.1016/j.canlet.2019.11.029. Epub 2019 Nov 26.

Authors

Tianqiang Jin¹, Chao Wang², Yu Tian¹, Chaoliu Dai¹, Yuwen Zhu³, Feng Xu⁴

Affiliations

¹ Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 110004, China.
² Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 110004, China; Department of Surgery, Northeast International Hospital, Shenyang, 110623, China.
³ Department of Surgery, University of Colorado Anschutz Medical Campus, Aurora, CO, 80045, USA.
⁴ Department of General Surgery, Shengjing Hospital of China Medical University, Shenyang, 110004, China. Electronic address: xufengsjh@163.com.

PMID: 31783085
DOI: 10.1016/j.canlet.2019.11.029

Abstract

Mitochondria are known as essential biosynthetic, bioenergetic and signaling organelles, and play a critical role in cell differentiation, proliferation, and death. Nowadays, cancer is emergingly considered as a mitochondrial metabolic disease. Mitochondria also play an essential role in liver carcinogenesis. Liver cells are highly regenerative and require high energy. For that reason, a large number of mitochondria are present and functional in liver cells. Abnormalities in mitochondrial metabolism in human liver are known to be one of the carcinogenic factors. Interestingly, immune checkpoints regulate mitochondrial metabolic energetics of the tumor, the tumor microenvironment, as well as the tumor-specific immune response. This regulation forms a positive loop between the metabolic reprogramming of both cancer cells and immune cells. In this review, we discuss the evidence and mechanisms that mitochondria interplay with immune checkpoints to influence different steps of oncogenesis, as well as the potential of mitochondria as therapeutic targets for liver cancer therapy.

Keywords: Immune checkpoint; Liver cancer; Mitochondria; Therapeutic target.

Publication types

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

MeSH terms

Animals
Antineoplastic Agents, Immunological / pharmacology
Antineoplastic Agents, Immunological / therapeutic use*
CTLA-4 Antigen / antagonists & inhibitors
CTLA-4 Antigen / immunology
CTLA-4 Antigen / metabolism
Carcinogenesis / drug effects
Carcinogenesis / immunology
Carcinogenesis / pathology*
Clinical Trials as Topic
Disease Models, Animal
Disease Progression
Energy Metabolism / drug effects*
Energy Metabolism / immunology
Humans
Liver / cytology
Liver / immunology
Liver / pathology
Liver Neoplasms / drug therapy
Liver Neoplasms / pathology*
Mitochondria / drug effects
Mitochondria / immunology
Mitochondria / metabolism*
Neoplastic Stem Cells / drug effects
Neoplastic Stem Cells / immunology
Neoplastic Stem Cells / metabolism
Neoplastic Stem Cells / pathology
Oxidative Phosphorylation / drug effects
Programmed Cell Death 1 Receptor / antagonists & inhibitors
Programmed Cell Death 1 Receptor / immunology
Programmed Cell Death 1 Receptor / metabolism
Signal Transduction / drug effects
Signal Transduction / immunology
Treatment Outcome
Tumor Microenvironment / drug effects
Tumor Microenvironment / immunology

Substances

Antineoplastic Agents, Immunological
CTLA-4 Antigen
CTLA4 protein, human
PDCD1 protein, human
Programmed Cell Death 1 Receptor