학술논문

Targeting the AAA ATPase p97 as an Approach to Treat Cancer through Disruption of Protein Homeostasis
Document Type
article
Source
Cancer Cell. 28(5)
Subject
Biochemistry and Cell Biology
Biomedical and Clinical Sciences
Biological Sciences
Biotechnology
Cancer
Genetics
2.1 Biological and endogenous factors
Aetiology
Adenosine Triphosphatases
Animals
Apoptosis
Blotting
Western
CRISPR-Cas Systems
Cell Line
Tumor
Endoplasmic Reticulum-Associated Degradation
Enzyme Inhibitors
Gene Expression Regulation
Neoplastic
HCT116 Cells
HEK293 Cells
Homeostasis
Humans
Indoles
K562 Cells
Mice
Nude
Mice
SCID
Molecular Structure
Molecular Targeted Therapy
Neoplasms
Nuclear Proteins
Pyrimidines
RNA Interference
Reverse Transcriptase Polymerase Chain Reaction
Ubiquitinated Proteins
Xenograft Model Antitumor Assays
Neurosciences
Oncology and Carcinogenesis
Oncology & Carcinogenesis
Biochemistry and cell biology
Oncology and carcinogenesis
Language
Abstract
p97 is a AAA-ATPase with multiple cellular functions, one of which is critical regulation of protein homeostasis pathways. We describe the characterization of CB-5083, a potent, selective, and orally bioavailable inhibitor of p97. Treatment of tumor cells with CB-5083 leads to accumulation of poly-ubiquitinated proteins, retention of endoplasmic reticulum-associated degradation (ERAD) substrates, and generation of irresolvable proteotoxic stress, leading to activation of the apoptotic arm of the unfolded protein response. In xenograft models, CB-5083 causes modulation of key p97-related pathways, induces apoptosis, and has antitumor activity in a broad range of both hematological and solid tumor models. Molecular determinants of CB-5083 activity include expression of genes in the ERAD pathway, providing a potential strategy for patient selection.