ArticleAnnals of translational medicine2021
PSMD12 promotes glioma progression by upregulating the expression of Nrf2.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- PSMD8 promotes breast cancer progression and attenuates paclitaxel sensitivity by stabilizing KIF10.Cancer cell international · 2026Article
- PSMD12 Overexpression Promotes Lung Adenocarcinoma Progression via Ubiquitin-Proteasome Pathway Dysregulation.Cancer science · 2026Article
- Dysregulation of post-translational modifications in glioma: advances in pathological mechanisms and clinical targeting strategies.Journal of translational medicine · 2026Review
- Metabolic-transcriptional rewiring by NFE2L2 promotes M2 macrophage polarization and anti-PD-L1 resistance in glioma.Cancer cell international · 2025Article
- Integrating multi-omics to unveil PSMD12 as a critical gene in promoting brain metastases of lung adenocarcinoma.Journal of translational medicine · 2025Article
- NRF2-mediated autophagic degradation of glycated vimentin in the skin by an elastin-derived peptide.American journal of translational research · 2025Article
- NSP6 inhibits the production of ACE2-containing exosomes to promote SARS-CoV-2 infectivity.mBio · 2024Article
- PSMB2 plays an oncogenic role in glioma and correlates to the immune microenvironment.Scientific reports · 2024Article
- PSMD12 promotes non-small cell lung cancer progression through activating the Nrf2/TrxR1 pathway.Genes & genomics · 2024Article
- CSF2 Impairs Nrf2 Signaling through the Akt/Mtor Pathway in the Development of Bladder Cancer.Journal of Cancer · 2024Article
- Role of Glycolytic and Glutamine Metabolism Reprogramming on the Proliferation, Invasion, and Apoptosis Resistance through Modulation of Signaling Pathways in Glioblastoma.International journal of molecular sciences · 2023Review
- PSMD12 interacts with CDKN3 and facilitates pancreatic cancer progression.Cancer gene therapy · 2023Article
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- PSMD12 promotes the activation of the MEK-ERK pathway by upregulating KIF15 to promote the malignant progression of liver cancer.Cancer biology & therapy · 2022Article
- The Role of NRF2/KEAP1 Pathway in Glioblastoma: Pharmacological Implications.Medical oncology (Northwood, London, England) · 2022Review
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Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioma is the most common and aggressive primary brain tumor in adults. Proteasome 26S subunit, non-ATPase 12 (PSMD12), an important subunit in the 26S proteasome, is known to be involved in the growth and apoptosis of breast cancer cells. However, its exact function and underlying molecular mechanisms in glioma remain unknown.
methodsPSMD12 expression was detected in glioma tissue specimens by immunohistochemistry (IHC) and TCGA database. Overexpression and down-regulation of PSMD12 and Nrf2 were induced in glioma cell lines, and CCK-8 and Transwell assays were used to detect cell proliferation and invasion evaluation, respectively. Xenograft model was used to observe the effect of knockdown of PSMD12 on tumor growth. Immunohistochemical assays and TCGA database were conducted to reveal the relationships between PSMD12 expression and Nrf2. Finally, Western blot and related biological function experiments were used to explore the mechanism of PSMD12 regulating the glioma progression and Nrf2.
resultsWe revealed that PSMD12 is upregulated in glioma, especially in high-grade glioma, by analyzing bioinformatics data and clinical specimens. PSMD12 upregulation was associated with poor prognosis in glioma patients. Knockdown of PSMD12 inhibited the growth of glioma cells
conclusionsThese results suggest that PSMD12 is considered to be a crucial regulator of the development and progression of glioma and may serve as a potential biomarker or therapeutic target for the treatment of glioma.
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