Depletion of COPI in cancer cells: the role of reactive oxygen species in the induction of lipid accumulation, noncanonical lipophagy and apoptosis-Reference-Cited by-同舟云学术

Depletion of COPI in cancer cells: the role of reactive oxygen species in the induction of lipid accumulation, noncanonical lipophagy and apoptosis

Published:2022-12-01 Issue:14 Volume:33 Page:
ISSN:1059-1524
Container-title:Molecular Biology of the Cell
language:en
Short-container-title:MBoC

Author:

Gasparian A.¹,Aksenova M.¹,Oliver D.¹,Levina E.²,Doran R.¹,Lucius M.¹,Piroli G.³,Oleinik N.⁴,Ogretmen B.⁴,Mythreye K.⁵,Frizzell N.³,Broude E.¹,Wyatt M. D.¹,Shtutman M.¹^ORCID

Affiliation:

1. Department of Drug Discovery and Biomedical Sciences, College of Pharmacy, University of South Carolina, Columbia, SC 29208

2. Department of Biological Sciences College of Art and Science, University of South Carolina, Columbia, SC 29208

3. Department of Pharmacology, Physiology & Neuroscience, School of Medicine, University of South Carolina, Columbia, SC 29208

4. Department of Biochemistry and Molecular Biology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425

5. Department of Pathology, Division of Molecular and Cellular Pathology, University of Alabama at Birmingham, Birmingham, AL 35233

Abstract

COPI depletion in tumor cells causes ROS accumulation and ROS-dependent formation of lipid droplets. ROS-dependent noncanonical lipophagy is marked by the accumulation of LC3-II and SQSTM1 and colocalization of the proteins with lipid droplets.

Publisher

American Society for Cell Biology (ASCB)

Subject

Cell Biology,Molecular Biology

Reference61 articles.

1. Dysfunction of pulmonary surfactant mediated by phospholipid oxidation is cholesterol-dependent

2. Targeting COPZ1 non-oncogene addiction counteracts the viability of thyroid tumor cells

3. Mutations in the COPI coatomer subunit α-COP induce release of Aβ-42 and amyloid precursor protein intracellular domain and increase tau oligomerization and release

4. Novel insights into pancreatic β-cell glucolipotoxicity from real-time functional analysis of mitochondrial energy metabolism in INS-1E insulinoma cells

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