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Proceedings 2018, 2(25), 1583; https://doi.org/10.3390/proceedings2251583

Proteasomal Inhibition with Bortezomib Causes Selective Autophagy Upregulation and Perinuclear Clustering of Mitochondria in Human Neuronal Cells

1
Department of Pharmaceutical Toxicology, Faculty of Pharmacy, Istanbul University, Istanbul 34126, Turkey
2
Genetic and Metabolic Diseases Research and Investigation Center, Marmara University, Istanbul 34854, Turkey
Presented at the 2nd International Cell Death Research Congress, Izmir, Turkey, 1–4 November 2018.
*
Author to whom correspondence should be addressed.
Published: 6 December 2018
PDF [1440 KB, uploaded 6 December 2018]

Abstract

The ubiquitin proteasomal system and autophagic pathway are two main protein degradation systems in eukaryotic cells. Inhibition of the proteasomal system with proteasome inhibitors for cancer treatment can cause neurotoxic side effects. In this study, we investigated neurotoxic side effects of bortezomib (BTZ) and carfilzomib (CFZ) in a human neuronal cell model. Inhibition of proteasome with BTZ upregulated autophagy receptor protein p62 level. BTZ caused reduced mitochondrial mass per cell in a greater extent than CFZ. BTZ caused more clustering of mitochondria than CFZ. In conclusion, mitochondrial toxicity and autophagic upregulation with BTZ may be the reason for more severe neurotoxic profile than CFZ.
Keywords: proteasome inhibitors; autophagy; mitochondrial toxicity proteasome inhibitors; autophagy; mitochondrial toxicity
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Jannuzzi, A.T.; Sari, G.; Yilmaz, A.M.; Karademir, B.; Alpertunga, B. Proteasomal Inhibition with Bortezomib Causes Selective Autophagy Upregulation and Perinuclear Clustering of Mitochondria in Human Neuronal Cells. Proceedings 2018, 2, 1583.

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