ER stress signaling at the interphase between MASH and HCC

Author:

Hazari Younis1234,Chevet Eric56ORCID,Bailly-Maitre Béatrice78ORCID,Hetz Claudio1239ORCID

Affiliation:

1. Program of Cellular and Molecular Biology, Institute of Biomedical Sciences, University of Chile, Santiago, Chile

2. Faculty of Medicine, Biomedical Neuroscience Institute (BNI), University of Chile, Santiago, Chile

3. Center for Geroscience, Brain Health and Metabolism (GERO), Santiago, Chile

4. Department of Biotechnology, University of Kashmir, Srinagar, India

5. Inserm U1242, University of Rennes, Rennes, France

6. Centre de Lutte Contre le Cancer Eugène Marquis, Rennes, France

7. Institut National de la Santé et de la Recherche Médicale (INSERM) UMR1065, Université Côte d’Azur (UCA), Centre Méditerranéen de Médecine Moléculaire (C3M), 06204 Nice, France Team “Metainflammation and Hematometabolism”, Metabolism Department, France

8. Université Côte d’Azur, INSERM, U1065, C3M, 06200 Nice, France

9. Buck Institute for Research on Aging, Novato, California, USA

Abstract

HCC is the most frequent primary liver cancer with an extremely poor prognosis and often develops on preset of chronic liver diseases. Major risk factors for HCC include metabolic dysfunction–associated steatohepatitis, a complex multifactorial condition associated with abnormal endoplasmic reticulum (ER) proteostasis. To cope with ER stress, the unfolded protein response engages adaptive reactions to restore the secretory capacity of the cell. Recent advances revealed that ER stress signaling plays a critical role in HCC progression. Here, we propose that chronic ER stress is a common transversal factor contributing to the transition from liver disease (risk factor) to HCC. Interventional strategies to target the unfolded protein response in HCC, such as cancer therapy, are also discussed.

Publisher

Ovid Technologies (Wolters Kluwer Health)

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