ArticleJournal of neuro-oncology2000
Protein kinase C zeta isoform is critical for proliferation in human glioblastoma cell lines.
Article in Journal of neuro-oncology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 39 citations in OpenAlex.
- Phase II and pharmacogenomics study of enzastaurin plus temozolomide during and following radiation therapy in patients with newly diagnosed glioblastoma multiforme and gliosarcoma.Neuro-oncology · 2011Trial
- Protein Kinase C (PKC) Isozymes as Diagnostic and Prognostic Biomarkers and Therapeutic Targets for Cancer.Cancers · 2022Review
- Baicalin Inhibits Human Cervical Cancer Cells by Suppressing Protein Kinase C/Signal Transducer and Activator of Transcription (PKC/STAT3) Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- STAT3 Serine 727 Phosphorylation: A Relevant Target to Radiosensitize Human Glioblastoma.Brain pathology (Zurich, Switzerland) · 2016Article
- Atypical protein kinase C zeta: potential player in cell survival and cell migration of ovarian cancer.PloS one · 2015Article
- PKC signaling in glioblastoma.Cancer biology & therapy · 2013Review
- Enzastaurin plus temozolomide with radiation therapy in glioblastoma multiforme: a phase I study.Neuro-oncology · 2010Article
- Review
- Dap160/intersectin binds and activates aPKC to regulate cell polarity and cell cycle progression.Development (Cambridge, England) · 2008Article
- Atypical protein kinase C regulates dual pathways for degradation of the oncogenic coactivator SRC-3/AIB1.Molecular cell · 2008Article
- Oncomine 3.0: genes, pathways, and networks in a collection of 18,000 cancer gene expression profiles.Neoplasia (New York, N.Y.) · 2007Article
- Regulation of glioma cell migration by serine-phosphorylated P311.Neoplasia (New York, N.Y.) · 2005Article
- Effects of the PKC inhibitor PD 406976 on cell cycle progression, proliferation, PKC isozymes and apoptosis in glioma and SVG-transformed glial cells.Cell proliferation · 2005Article
- Measurement of tamoxifen-induced apoptosis in glioblastoma by cytometric bead analysis of active caspase-3.Journal of neuro-oncologyArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have confirmed that proliferation in glioblastoma cell lines can be blocked by non-isoform specific protein kinase C (PKC) inhibitors, e.g calphostin C, staurosporine. However, the exact mechanism of PKC involvement is poorly understood. The aim of this study was to explore the role of specific PKC isoforms in the aberrant growth of glioblastoma. Identification of the isoform(s) critical for proliferation in glioblastoma would present a better target for the design of chemotherapeutic strategies. To this end, we screened expression on PKC isoforms in four human glioblastoma cell lines both when proliferating and in a quiescent state using western assays. PKC isoforms alpha, beta, betaII and zeta were found to be expressed in all cell lines. PKC epsilon was detected in three out of four cell lines and PKC eta was detected in one out of four cell lines. Quiescence of growth resulted in down-regulation of PKC epsilon. We examined the role of these isoforms by studying the effect of PKC isoform-specific inhibitors bisindolylmaleimide-I and Gö6976 on proliferation in a panel of four human glioblastoma cell lines. Inhibition of PKC alpha and epsilon had no effect on proliferation, suggesting that previous studies targeting PKC alpha may not be of therapeutic benefit. More significantly, it was shown that inhibition of PKC zeta blocked proliferation. This suggests that the inhibition of PKC zeta may be an important chemotherapeutic target for arresting growth in glioblastoma.
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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.