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Emerging Players in Autophagy Deficiency-Induced Liver Injury and Tumorigenesis

Hua Yang1, Hong-Min Ni2, Wen-Xing Ding2

  • 1Department of General Surgery, Shanghai Public Health Clinical Center, Fudan University, Shanghai, P.R. China.

Gene Expression
|February 6, 2019
PubMed

Insights

Defective autophagy acts as a tumor suppressor, promoting liver cancer in mice. Persistent Nrf2 activation, alongside HMGB1 and Yap, drives liver injury and tumor development in these models.

Area of Science:

  • Cell Biology
  • Oncology
  • Genetics

Background:

  • Macroautophagy/autophagy functions as a tumor suppressor, evidenced by liver tumors in Atg5/Atg7 knockout mice.
  • p62-mediated Nrf2 activation is implicated in autophagy deficiency-driven liver injury and tumorigenesis.
  • The precise mechanisms linking sustained Nrf2 activation to liver disease and cancer remain unclear.

Purpose of the Study:

  • To explore the roles of High Mobility Group Box 1 (HMGB1) and Yes1 Associated Transcriptional Regulator (Yap) in liver injury and tumorigenesis.
  • To elucidate the mechanisms underlying liver injury and cancer in mice with impaired autophagy.

Main Methods:

  • Utilizing liver-specific Atg5 or Atg7 knockout mouse models.
  • Investigating the involvement of HMGB1 and Yap in the context of autophagy deficiency.

Main Results:

  • Autophagy deficiency leads to spontaneous liver tumors in mice.
  • p62-mediated Nrf2 activation is crucial for liver injury and tumor development.
  • HMGB1 and Yap play significant roles in regulating liver injury and tumorigenesis in autophagy-deficient mice.

Conclusions:

  • Macroautophagy/autophagy is a critical tumor suppressor in the liver.
  • Targeting Nrf2, HMGB1, and Yap may offer therapeutic strategies for liver cancer prevention and treatment.

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