ArticleJournal of Cancer2016
Centrosomal Protein of 55 Regulates Glucose Metabolism, Proliferation and Apoptosis of Glioma Cells via the Akt/mTOR Signaling Pathway.
Article in Journal of Cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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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
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Prognostic significance of CEP55 expression in non-small cell lung cancer: a systematic review and meta-analysis.BMC pulmonary medicine · 2026Pooled it
- Correlation of the AKT/mTOR signaling pathway with the clinicopathological features and prognosis of nasopharyngeal carcinoma.European journal of histochemistry : EJH · 2021Trial
- HIST1H2BJ is associated with poor prognosis and an immune-altered tumor microenvironment in glioma.Frontiers in immunology · 2026Article
- Unveiling the significance of cancer-testis antigens and their implications for immunotherapy in glioma.Discover oncology · 2024Review
- Ang II Controls the Expression of Mapkap1 by miR-375 and Affects the Function of Islet β Cells.Endocrine, metabolic & immune disorders drug targets · 2023Article
- CEP55 3'-UTR promotes epithelial-mesenchymal transition and enhances tumorigenicity of bladder cancer cells by acting as a ceRNA regulating miR-497-5p.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Review
- LncRNA HOXA-AS2 promotes glioblastoma carcinogenesis by targeting miR-885-5p/RBBP4 axis.Cancer cell international · 2021Article
- Circular RNAs: A Promising Biomarker for Endometrial Cancer.Cancer management and research · 2021Review
- PART1 and hsa-miR-429-Mediated SHCBP1 Expression Is an Independent Predictor of Poor Prognosis in Glioma Patients.BioMed research international · 2020Article
- The value of CEP55 gene as a diagnostic biomarker and independent prognostic factor in LUAD and LUSC.PloS one · 2020Article
- Long non-coding RNA SNHG5 promotes glioma progression via miR-205/E2F3 axis.Bioscience reports · 2019Article
- The long non-coding RNA SNHG1 promotes glioma progression by competitively binding to miR-194 to regulate PHLDA1 expression.Cell death & disease · 2019Article
- Diagnostic and prognostic value of CEP55 in clear cell renal cell carcinoma as determined by bioinformatics analysis.Molecular medicine reports · 2019Article
- GNG7 silencing promotes the proliferation and differentiation of placental cytotrophoblasts in preeclampsia rats through activation of the mTOR signaling pathway.International journal of molecular medicine · 2019Article
- MicroRNA-524 inhibits the progress of glioma via the direct targeting of NCF2.American journal of translational research · 2019Article
- ROS generation and autophagosome accumulation contribute to the DMAMCL-induced inhibition of glioma cell proliferation by regulating the ROS/MAPK signaling pathway and suppressing the Akt/mTOR signaling pathway.OncoTargets and therapy · 2019Article
- Article
- CEP55 promotes cell proliferation and inhibits apoptosis via the PI3K/Akt/p21 signaling pathway in human glioma U251 cells.Oncology letters · 2018Article
- Overexpression of centrosomal protein 55 regulates the proliferation of glioma cell and mediates proliferation promoted by EGFRvIII in glioblastoma U251 cells.Oncology letters · 2018Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionGlioma is one of the most common and most aggressive brain tumors in humans. The molecular and cellular mechanisms responsible for the onset and the progression of glioma are elusive and controversial. Centrosomal protein of 55 (CEP55) was initially described as a highly coiled-coil protein that plays critical roles in cell division, but was recently identified as being overexpressed in many human cancers. The function of CEP55 has not previously been characterized in glioma. We aim to discover the effect and mechanism of CEP55 in glioma development.
methodqRT-PCR and immunohistochemistry were used to analyze CEP55 expression. Glucose uptake, western blot, MTS, CCK-8, Caspase-3 activity and TUNEL staining assays were performed to investigate the role and mechanism of CEP55 on glioma cell process.
resultsWe found that the levels of CEP55 expression were upregulated in glioma. In addition, CEP55 appeared to regulate glucose metabolism of glioma cells. Furthermore, knockdown of CEP55 inhibited cell proliferation and induced cell apoptosis in glioma. Finally, we provided preliminary evidence that knockdown of CEP55 inhibited glioma development via suppressing the activity of Akt/mTOR signaling.
conclusionsOur results demonstrated that CEP55 regulates glucose metabolism, proliferation and apoptosis of glioma cells via the Akt/mTOR signaling pathway, and its promotive effect on glioma tumorigenesis can be a potential target for glioma therapy in the future.
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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.