Long-term depletion of Cereblon induces mitochondrial dysfunction in cancer cells

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Title
Long-term depletion of Cereblon induces mitochondrial dysfunction in cancer cells
Author(s)
Seulki Park; K Kim; Keeok Haam; Hyun Seung BanJung Ae KimByoung Chul ParkSung Goo Park; Sunhong Kim; Jeong Hoon Kim
Bibliographic Citation
BMB Reports, vol. 54, no. 6, pp. 305-310
Publication Year
2021
Abstract
Cereblon (CRBN) is a multi-functional protein that acts as a substrate receptor of the E3 ligase complex and a molecular chaperone. While CRBN is proposed to function in mitochondria, its specific roles are yet to be established. Here, we showed that knockdown of CRBN triggers oxidative stress and calcium overload in mitochondria, leading to disruption of mitochondrial membrane potential. Notably, long-term CRBN depletion using PROteolysis TArgeting Chimera (PROTAC) induced irreversible mitochondrial dysfunction, resulting in cell death. Our collective findings indicate that CRBN is required for mitochondrial homeostasis in cells.
Keyword
Calcium overloadCell deathCRBNMitochondrial dysfunctionROS
ISSN
1976-6696
DOI
http://dx.doi.org/10.5483/BMBRep.2021.54.6.218
Type
Article
Appears in Collections:
Division of Biomedical Research > Biotherapeutics Translational Research Center > 1. Journal Articles
Division of Biomedical Research > Personalized Genomic Medicine Research Center > 1. Journal Articles
Division of Biomedical Research > Disease Target Structure Research Center > 1. Journal Articles
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