ArticlePloS one2010
Co-depletion of cathepsin B and uPAR induces G0/G1 arrest in glioma via FOXO3a mediated p27 upregulation.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 19 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.
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
19 citing papers in PubMed, 27 citations in OpenAlex.
- Loss of p27Kip1 leads to expansion of CD4+ effector memory T cells and accelerates colitis-associated colon cancer in mice with a T cell lineage restricted deletion of Smad4.Oncoimmunology · 2020Article
- Retraction: Co-Depletion of Cathepsin B and uPAR Induces G0/G1 Arrest in Glioma via FOXO3a Mediated p27Kip1 Upregulation.PloS one · 2020Article
- Receptor tyrosine kinase-Ras-PI 3 kinase-Akt signaling network in glioblastoma multiforme.Medical oncology (Northwood, London, England) · 2018Review
- Review
- Icariside II induces cell cycle arrest and apoptosis in human glioblastoma cells through suppressing Akt activation and potentiating FOXO3a activity.American journal of translational research · 2017Article
- Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: focus on the cancer hallmark of tumor angiogenesis.Carcinogenesis · 2015Review
- Cathepsin B-deficient mice as source of monoclonal anti-cathepsin B antibodies.Biological chemistry · 2015Article
- CELF1 is Up-Regulated in Glioma and Promotes Glioma Cell Proliferation by Suppression of CDKN1B.International journal of biological sciences · 2015Article
- Knockdown of cathepsin B and uPAR inhibits CD151 and α3β1 integrin-mediated cell adhesion and invasion in glioma.Molecular carcinogenesis · 2013Article
- Platelet-derived growth factor-A regulates lung fibroblast S-phase entry through p27(kip1) and FoxO3a.Respiratory research · 2013Article
- Cathepsin B as a cancer target.Expert opinion on therapeutic targets · 2013Review
- uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells.International journal of oncology · 2012Article
- uPAR and cathepsin B inhibition enhanced radiation-induced apoptosis in gliomainitiating cells.Neuro-oncology · 2012Article
- uPAR and cathepsin B downregulation induces apoptosis by targeting calcineurin A to BAD via Bcl-2 in glioma.Journal of neuro-oncology · 2012Article
- MMP-9 silencing regulates hTERT expression via β1 integrin-mediated FAK signaling and induces senescence in glioma xenograft cells.Cellular signalling · 2011Article
- Mechanism of p27 upregulation induced by downregulation of cathepsin B and uPAR in glioma.Molecular oncology · 2011Article
- Inhibition of cathepsin B activity attenuates extracellular matrix degradation and inflammatory breast cancer invasion.Breast cancer research : BCR · 2011Article
- Regulation of DNA repair mechanism in human glioma xenograft cells both in vitro and in vivo in nude mice.PloS one · 2011Article
- Article
Corrections and comments
- Retraction · 2020-01-29Concerns/Issues about Image · Duplication of/in Image · Manipulation of Images · · Jasti S Rao has institutional finding of misconduct;
- Retracted
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCathepsin B and urokinase plasminogen activator receptor (uPAR) are both known to be overexpressed in gliomas. Our previous work and that of others strongly suggest a relationship between the infiltrative phenotype of glioma and the expression of cathepsin B and uPAR. Though their role in migration and adhesion are well studied the effect of these molecules on cell cycle progression has not been thoroughly examined. METHODOLOGY/PRINCIPAL
findingsCathepsin B and uPAR single and bicistronic siRNA plasmids were used to downregulate these molecules in SNB19 and U251 glioma cells. FACS analysis and BrdU incorporation assay demonstrated G0/G1 arrest and decreased proliferation with the treatments, respectively. Immunoblot and immunocyto analysis demonstrated increased expression of p27(Kip1) and its nuclear localization with the knockdown of cathepsin B and uPAR. These effects could be mediated by alphaVbeta3/PI3K/AKT/FOXO pathway as observed by the decreased alphaVbeta3 expression, PI3K and AKT phosphorylation accompanied by elevated FOXO3a levels. These results were further confirmed with the increased expression of p27(Kip1) and FOXO3a when treated with Ly294002 (10 microM) and increased luciferase expression with the siRNA and Ly294002 treatments when the FOXO binding promoter region of p27(Kip1) was used. Our treatment also reduced the expression of cyclin D1, cyclin D2, p-Rb and cyclin E while the expression of Cdk2 was unaffected. Of note, the Cdk2-cyclin E complex formation was reduced significantly. CONCLUSION/SIGNIFICANCE: Our study indicates that cathepsin B and uPAR knockdown induces G0/G1 arrest by modulating the PI3K/AKT signaling pathway and further increases expression of p27(Kip1) accompanied by the binding of FOXO3a to its promoter. Taken together, our findings provide molecular mechanism for the G0/G1 arrest induced by the downregulation of cathepsin B and uPAR in SNB19 and U251 glioma 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.