ArticleOncotarget2016
Downregulation of 26S proteasome catalytic activity promotes epithelial-mesenchymal transition.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- The proteasome as a druggable target with multiple therapeutic potentialities: Cutting and non-cutting edges.Pharmacology & therapeutics · 2020Pooled it
- Targeting the Molecules in EMT: A Potential Therapeutic Opportunity in Breast Cancer.Current molecular medicine · 2025Review
- Exosomal misfolded proteins released by cancer stem cells: dual functions in balancing protein homeostasis and orchestrating tumor progression.Discover oncology · 2024Review
- Integrative analysis reveals early epigenetic alterations in high-grade serous ovarian carcinomas.Experimental & molecular medicine · 2023Article
- Article
- Genome-Wide Analysis of lncRNA-mRNA Co-Expression Networks in CD133+/CD44+ Stem-like PDAC Cells.Cancers · 2023Article
- Applications of single-cell sequencing in cancer research: progress and perspectives.Journal of hematology & oncology · 2021Review
- Proteasome Complexes and Their Heterogeneity in Colorectal, Breast and Pancreatic Cancers.Journal of Cancer · 2021Article
- Targeting poor proteasomal function with radioiodine eliminates CT26 colon cancer stem cells resistant to bortezomib therapy.Scientific reports · 2020Article
- Hakin-1, a New Specific Small-Molecule Inhibitor for the E3 Ubiquitin-Ligase Hakai, Inhibits Carcinoma Growth and Progression.Cancers · 2020Article
- The Role of Cancer Stem Cells in Radiation Resistance.Frontiers in oncology · 2020Review
- Single-cell RNA-sequencing of migratory breast cancer cells: discovering genes associated with cancer metastasis.The Analyst · 2019Article
- E-cadherin-Fc chimera protein matrix enhances cancer stem-like properties and induces mesenchymal features in colon cancer cells.Cancer science · 2019Article
- Proteasomes and Several Aspects of Their Heterogeneity Relevant to Cancer.Frontiers in oncology · 2019Review
- Quantitative peptidomics of endogenous peptides involved in TGF-β1-induced epithelial mesenchymal transition of renal epithelial cells.Cell death discovery · 2018Article
- Epithelial-Mesenchymal Transition and Metastasis under the Control of Transforming Growth Factor β.International journal of molecular sciences · 2018Review
- USP11 Enhances TGFβ-Induced Epithelial-Mesenchymal Plasticity and Human Breast Cancer Metastasis.Molecular cancer research : MCR · 2018Article
- Galectin-8 induces partial epithelial-mesenchymal transition with invasive tumorigenic capabilities involving a FAK/EGFR/proteasome pathway in Madin-Darby canine kidney cells.Molecular biology of the cell · 2018Article
- Hakai overexpression effectively induces tumour progression and metastasis in vivo.Scientific reports · 2018Article
- Proteasome activity regulates CD8+ T lymphocyte metabolism and fate specification.The Journal of clinical investigation · 2017Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
The epithelial-mesenchymal transition (EMT) endows carcinoma cells with phenotypic plasticity that can facilitate the formation of cancer stem cells (CSCs) and contribute to the metastatic cascade. While there is substantial support for the role of EMT in driving cancer cell dissemination, less is known about the intracellular molecular mechanisms that govern formation of CSCs via EMT. Here we show that β2 and β5 proteasome subunit activity is downregulated during EMT in immortalized human mammary epithelial cells. Moreover, selective proteasome inhibition enabled mammary epithelial cells to acquire certain morphologic and functional characteristics reminiscent of cancer stem cells, including CD44 expression, self-renewal, and tumor formation. Transcriptomic analyses suggested that proteasome-inhibited cells share gene expression signatures with cells that have undergone EMT, in part, through modulation of the TGF-β signaling pathway. These findings suggest that selective downregulation of proteasome activity in mammary epithelial cells can initiate the EMT program and acquisition of a cancer stem cell-like phenotype. As proteasome inhibitors become increasingly used in cancer treatment, our findings highlight a potential risk of these therapeutic strategies and suggest a possible mechanism by which carcinoma cells may escape from proteasome inhibitor-based therapy.
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What OpenQuestion holds
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.