ArticleScientific reports2022
Prolonged treatment with the proteasome inhibitor MG-132 induces apoptosis in PC12 rat pheochromocytoma cells.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Natural sesquiterpene lactones in prostate cancer therapy: mechanisms and sources.Medical oncology (Northwood, London, England) · 2025Review
- Graphene Nanocomposites in the Targeting Tumor Microenvironment: Recent Advances in TME Reprogramming.International journal of molecular sciences · 2025Review
- Proteasome inhibitor MG132 modulates signal transduction pathways in ELT3 uterine leiomyoma cells.Experimental and therapeutic medicine · 2025Article
- Targeting Microglial Immunoproteasome: A Novel Approach in Neuroinflammatory-Related Disorders.ACS chemical neuroscience · 2024Review
- Post-Translational Modifications in Tau and Their Roles in Alzheimer's Pathology.Current Alzheimer research · 2024Review
- Neuroprotective Effects of Licochalcone D in Oxidative-Stress-Induced Primitive Neural Stem Cells from Parkinson's Disease Patient-Derived iPSCs.Biomedicines · 2023Article
- Article
- MG132 protects against lung injury following brain death in rats.Experimental and therapeutic medicine · 2022Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rat pheochromocytoma (PC12) cells were treated with the proteasome inhibitor MG-132 and morphological changes were recorded. Initially, neuronal differentiation was induced but after 24 h signs of morphological deterioration became apparent. We performed nuclear staining, flow cytometry and WST-1 assay then analyzed signal transduction pathways involving Akt, p38 MAPK (Mitogen-Activated Protein Kinase), JNK (c-Jun N-terminal Kinase), c-Jun and caspase-3. Stress signaling via p38, JNK and c-Jun was active even after 24 h of MG-132 treatment, while the survival-mediating Akt phosphorylation declined and the executor of apoptosis (caspase-3) was activated by that time and apoptosis was also observable. We examined subcellular localization of stress signaling components, applied kinase inhibitors and dominant negative H-Ras mutant-expressing PC12 cells in order to decipher connections of stress-mediating pathways. Our results are suggestive of that treatment with the proteasome inhibitor MG-132 has a biphasic nature in PC12 cells. Initially, it induces neuronal differentiation but prolonged treatments lead to apoptosis.
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