ArticleCell proliferation2008
Involvement of PKC-iota in glioma proliferation.
Article in Cell proliferation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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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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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Sphingosine 1-phosphate (S1P) signaling in glioblastoma multiforme-A systematic review.International journal of molecular sciences · 2017Pooled it
- Impact of deleterious missense PRKCI variants on structural and functional dynamics of protein.Scientific reports · 2022Article
- Atypical PKCs activate Vimentin to facilitate prostate cancer cell motility and invasion.Cell adhesion & migration · 2021Article
- Simultaneous inhibition of atypical protein kinase‑C and mTOR impedes bladder cancer cell progression.International journal of oncology · 2020Article
- Semi-Synthetic Ingenol Derivative from Euphorbia tirucalli Inhibits Protein Kinase C Isotypes and Promotes Autophagy and S-phase Arrest on Glioma Cell Lines.Molecules (Basel, Switzerland) · 2019Article
- Preclinical testing of 5-amino-1-((1R,2S,3S,4R)-2,3-dihydroxy-4-methylcyclopentyl)-1H-imidazole-4-carboxamide: a potent protein kinase C-ι inhibitor as a potential prostate carcinoma therapeutic.Anti-cancer drugs · 2019Article
- Inhibition of atypical protein kinase C‑ι effectively reduces the malignancy of prostate cancer cells by downregulating the NF-κB signaling cascade.International journal of oncology · 2018Article
- Measuring the lactate-to-creatine ratio viaCellular & molecular biology letters · 2018Article
- Oncogenic PKC-ι activates Vimentin during epithelial-mesenchymal transition in melanoma; a study based on PKC-ι and PKC-ζ specific inhibitors.Cell adhesion & migration · 2018Article
- Two novel atypical PKC inhibitors; ACPD and DNDA effectively mitigate cell proliferation and epithelial to mesenchymal transition of metastatic melanoma while inducing apoptosis.International journal of oncology · 2017Article
- Targeting oncogenic protein kinase Cι for treatment of mutant KRAS LADC.Small GTPases · 2017Article
- Radiosensitization of human glioma cells by tamoxifen is associated with the inhibition of PKC-ι activityOncology letters · 2015Article
- Radiation-induced glioblastoma signaling cascade regulates viability, apoptosis and differentiation of neural stem cells (NSC).Apoptosis : an international journal on programmed cell death · 2014Article
- The interruption of PKC-ι signaling and TRAIL combination therapy against glioblastoma cells.Neurochemical research · 2014Article
- PKCλ/ι signaling promotes triple-negative breast cancer growth and metastasis.Cell death and differentiation · 2014Article
- Regulation of polarized morphogenesis by protein kinase C iota in oncogenic epithelial spheroids.Carcinogenesis · 2014Article
- PKC signaling in glioblastoma.Cancer biology & therapy · 2013Review
- Atypical protein kinase C phosphorylates Par6 and facilitates transforming growth factor β-induced epithelial-to-mesenchymal transition.Molecular and cellular biology · 2013Article
- High expression of KIBRA in low atypical protein kinase C-expressing gastric cancer correlates with lymphatic invasion and poor prognosis.Cancer science · 2013Article
- Regulation of Cdk7 activity through a phosphatidylinositol (3)-kinase/PKC-ι-mediated signaling cascade in glioblastoma.Carcinogenesis · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledAtypical protein kinase C-iota (PKC-iota) protects cells against apoptosis and may play a role in cell proliferation. However, in vivo, the status and function of PKC-iota in human normal brain tissue, gliomas, benign and malignant meningiomas as well as its in vitro status in proliferating and confluent glioma cells, remains unknown.
objectivesThe objectives of our research were to determine whether expression of PKC-iota is altered either in gliomas or in benign and malignant meningiomas, compared to normal brain. In addition, we wished to establish the expression of PKC-iota in proliferating plus in cell cycle-arrested glioma cell lines, as well as the relationship between PKC-iota siRNA on PKC-iota protein content and cell proliferation. MATERIALS AND
methodsWestern blot analyses for PKC-iota were performed on 12 normal brain biopsies, 15 benign meningiomas, three malignant meningiomas and three gliomas.
resultsResults demonstrated no (n = 9) or very weak (n = 3) detection of PKC-iota in normal brain tissue. In comparison, PKC-iota was robustly present in the majority of the benign meningiomas. Similarly, PKC-iota was abundant in all malignant meningiomas and gliomas. Western blotting for PKC-iota in confluent or proliferating glioma cell lines depicted substantial quantities of PKC-iota in proliferating T98G and U-138MG glioma cells. In contrast, confluent cells had either 71% (T98G) or 21% (U-138MG) less PKC-iota than proliferating cells. T98 and U-138 MG glioma cells treated with 100 nm PKC-iota siRNA had lower levels of cell proliferation compared to control siRNA-A and complete down-regulation of PKC-iota protein content.
conclusionThese results support the concept that presence of PKC-iota may be required for cell proliferation to take place.
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Registered trials
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