ArticleCancer research2018
PSMD5 Inactivation Promotes 26S Proteasome Assembly during Colorectal Tumor Progression.
Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- Mapping Interaction of Assembly Factor Rpn14 With the Proteasome Base Reveals a Bipartite Interface and Implies Ordered Remodeling of Intersubunit Contacts During Proteasome Biogenesis.Journal of molecular biology · 2026Article
- An Integrated Cardiac Microtissue Proteome Map Extends Therapeutic Remodeling by Nanovesicles.Molecular & cellular proteomics : MCP · 2026Article
- Structures of dynamic interactors at native proteasomes by PhIX-MS and cryo-electron microscopy.Molecular cell · 2026Article
- Transcriptome remodeling of mouse hearts during postnatal cardiac maturation and under proteotoxic stress.Molecular biology reports · 2026Article
- PACT is requisite for prostate cancer cell proliferation.Scientific reports · 2025Article
- More 26S and 30S proteasomes are beneficial in proteinopathy.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- miR-326 overexpression inhibits colorectal cancer cell growth and proteasome activity by targeting PNO1: unveiling a novel therapeutic intervention strategy.Scientific reports · 2024Article
- A telomere-related gene risk model for predicting prognosis and treatment response in acute myeloid leukemia.Heliyon · 2024Article
- HSPD1 Supports Osteosarcoma Progression through Stabilizing ATP5A1 and thus Activation of AKT/mTOR Signaling.International journal of biological sciences · 2024Article
- Gastric cancer cell types display distinct proteasome/immunoproteasome patterns associated with migration and resistance to proteasome inhibitors.Journal of cancer research and clinical oncology · 2023Article
- Article
- Multi-level characteristics recognition of cancer core therapeutic targets and drug screening for a broader patient population.Frontiers in pharmacology · 2023Article
- Hsp70 and Hsp110 Chaperones Promote Early Steps of Proteasome Assembly.Biomolecules · 2022Article
- Construction of the coexpression network involved in the pathogenesis of thyroid eye disease via bioinformatics analysis.Human genomics · 2022Article
- Discriminating Potential Genetic Markers for Complete Response and Non-Complete Response Patients to Neoadjuvant Chemotherapy with Locally Advanced Rectal Cancer.International journal of environmental research and public health · 2022Article
- Allele-specific genomic data elucidate the role of somatic gain and copy-number neutral loss of heterozygosity in cancer.Cell systems · 2022Article
- The Safety and Efficacy of Tofacitinib in 24 Cases of Pediatric Rheumatic Diseases: Single Centre Experience.Frontiers in pediatrics · 2022Article
- Article
- Kinectin1 depletion promotes EGFR degradation via the ubiquitin-proteosome system in cutaneous squamous cell carcinoma.Cell death & disease · 2021Article
- Erythroid mitochondrial retention triggers myeloid-dependent type I interferon in human SLE.Cell · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Protein degradation by the ubiquitin-proteasome system (UPS) is central to protein homeostasis and cell survival. The active 26S proteasome is a large protease complex consisting of a catalytic 20S subunit and 19S regulatory particles. Cancer cells are exposed to considerable protein overload due to high metabolic rates, reprogrammed energy metabolism, and aneuploidy. Here we report a mechanism that facilitates the assembly of active 26S proteasomes in malignant cells. Upon tumorigenic transformation of the gut epithelium, 26S proteasome assembly was significantly enhanced, but levels of individual subunits were not changed. This enhanced assembly of 26S proteasomes increased further with tumor progression and was observed specifically in transformed cells, but not in other rapidly dividing cells. Moreover, expression of PSMD5, an inhibitor of proteasome assembly, was reduced in intestinal tumors and silenced with tumor progression. Reexpression of PSMD5 in tumor cells caused decreased 26S assembly and accumulation of polyubiquitinated proteins. These results suggest that inhibition of cancer-associated proteasome assembly may provide a novel therapeutic strategy to selectively kill cancer cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.