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Updated: Jun 2, 2026

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis

An Oncogenic Hepatocyte-Induced Orthotopic Mouse Model of Hepatocellular Cancer Arising in the Setting of Hepatic Inflammation and Fibrosis

Published on: September 12, 2019

Autophagy-deficient mice develop multiple liver tumors.

Akito Takamura¹, Masaaki Komatsu, Taichi Hara

¹Department of Physiology and Cell Biology, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.

Genes & Development

|April 19, 2011

Summary

Autophagy, a cellular degradation process, prevents liver tumor formation in mice. Blocking autophagy leads to liver adenomas, and p62 accumulation worsens tumor growth, highlighting autophagy

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Area of Science:

Cellular Biology
Oncology
Molecular Biology

Background:

Autophagy is a fundamental cellular process responsible for degrading damaged proteins and organelles.
Autophagy plays a crucial role in maintaining cellular homeostasis and has been linked to tumor suppression.
Dysregulation of autophagy is increasingly recognized in various pathologies, including cancer.

Purpose of the Study:

To investigate the role of autophagy in the suppression of spontaneous liver tumorigenesis.
To elucidate the cellular mechanisms by which autophagy deficiency contributes to tumor development.
To assess the impact of p62, a key autophagy substrate, on tumor progression in the absence of autophagy.

Main Methods:

Generated mice with systemic mosaic deletion of Atg5 (autophagy-related gene 5).
Created liver-specific Atg7 knockout (Atg7⁻/⁻) mice to study liver tumorigenesis.
Analyzed tumor characteristics, including mitochondrial morphology, p62 levels, oxidative stress, and genomic damage.

Main Results:

Mice with Atg5 deletion and liver-specific Atg7 deficiency developed benign liver adenomas.
Tumor cells exhibited hallmarks of autophagy deficiency: mitochondrial swelling, p62 accumulation, and increased oxidative stress and genomic damage.
Simultaneous deletion of p62 significantly reduced the size of Atg7⁻/⁻ liver tumors, indicating p62's role in tumor progression.

Conclusions:

Autophagy is essential for the cell-intrinsic suppression of spontaneous tumorigenesis, particularly in the liver.
Autophagy deficiency in hepatocytes leads to mitochondrial dysfunction, oxidative stress, and genomic instability, promoting tumor initiation.
Accumulation of p62 is a key mechanism through which autophagy deficiency drives liver tumor progression.