ArticleTranslational cancer research2021
Down-regulation of PSMD4 can attenuate autophagy, enhance the accumulation of intracellular ROS, and increase the sensitivity of epithelial ovarian cancer to carboplatin by inhibiting the NF-κB pathway.
Article in Translational cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- A Narrative Review of In Vivo Studies on the Role of Reactive Oxygen Species in Ovarian Cancer.Antioxidants (Basel, Switzerland) · 2026Review
- Metabolic reprogramming-associated genomic instability drives colorectal cancer progression via the UBXN1-NF-κB axis.American journal of translational research · 2026Article
- PSMD4 Alleviates Aβ₁₋₄₂-Induced Mitochondrial Dysfunction and Oxidative Stress via the PGC-1α/Nrf Axis in Alzheimer's Disease Models.Molecular neurobiology · 2025Article
- "Double-edged sword" effect of reactive oxygen species (ROS) in tumor development and carcinogenesis.Physiological research · 2023Review
- Role of autophagy and its regulation by noncoding RNAs in ovarian cancer.Experimental biology and medicine (Maywood, N.J.) · 2023Review
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
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Abstract
backgroundThe incidence of ovarian cancer ranks third among female gynecological cancers in the world, and more than 90% of patients are epithelial ovarian cancer (EOC). Carboplatin is the first-line chemotherapy drug for the treatment of EOC patients. However, patients who are resistant to carboplatin often do not benefit from it. Therefore, finding a key molecule that affects carboplatin sensitivity is expected to enhance the efficacy of carboplatin in EOC treatment.
methodsThe human EOC cell line SK-OV-3 and TOV-21G were used in this study. The second-generation sequencing technology was used to sequence the transcripts of carboplatin-resistant EOC cells and parental EOC cells. The bioinformatic analysis of the differentially expressed genes was performed by Gene Ontology (GO) enrichment, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. The EOC tissue chip in the Gene Expression Omnibus (GEO) database was also analyzed to screen the target gene. Flow cytometry, Hoechst staining, Western blot, MTS, mitochondrial specific reducing agent (Mito Tempo), and nuclear factor kappa-B (NF-κB) pathway inhibitor (BAY 11-7082) were used to explore the effect of proteasome 26S subunit, non-ATPase 4 (PSMD4) on the autophagy, apoptosis, and reactive oxygen species (ROS) accumulation of carboplatin-resistant EOC cells treated with carboplatin.
resultsBased on second-generation sequencing technology and bioinformatics analysis, it was found that PSMD4 is the core molecule in the carboplatin resistance regulatory network in EOC, and its expression is up-regulated in EOC carboplatin-resistant tissues and cells.
conclusionsDown-regulation of PSMD4 may inhibit the activation of the NF-κB pathway and autophagy, and up-regulate the level of intracellular ROS accumulation, thereby promoting carboplatin-mediated EOC cell apoptosis and enhancing carboplatin sensitivity.
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