ArticleOncology letters2019
Overexpression of EPAC2 reduces the invasion of glioma cells via MMP-2.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 4 citations in OpenAlex.
- The Pivotal Role of Irradiation-induced Autophagy Mechanisms in Glioma Therapy.Anti-cancer agents in medicinal chemistry · 2025Review
- C3G Protein, a New Player in Glioblastoma.International journal of molecular sciences · 2021Review
- The Pivotal Immunomodulatory and Anti-Inflammatory Effect of Histone-Lysine N-Methyltransferase in the Glioma Microenvironment: Its Biomarker and Therapy Potentials.Analytical cellular pathology (Amsterdam) · 2021Review
- EPAC2: A new and promising protein for glioma pathogenesis and therapy.Oncology reviews · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exchange proteins directly activated by cAMP (EPACs) are crucial cyclic adenosine 3',5'-monophosphate- determined signaling pathway intercessors, which are associated with the pathogenesis of neurological disorders and numerous human diseases. To the best of our knowledge, the role of EPAC2 signaling via matrix metalloproteinase 2 (MMP-2) in the pathogenesis of glioma has not been studied. Therefore, the present study focused on the role of EPAC2 in glioma, and assessed the invasiveness of human glioma cell lines following EPAC2 overexpression. Expression levels of EPAC2 in normal brain tissues and clinical glioma specimens were detected by western blotting. An EPAC2 overexpression vector was transfected into U251 and U87 cell lines to increase the expression levels of EPAC2. Expression levels of MMP-2 were detected by western blotting, and the invasive abilities of glioma cells were detected by a Transwell assay. EPAC2 was relatively highly expressed in normal brain tissue, while EPAC2 expression was significantly decreased in clinical glioma specimens (P<0.01).
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Registered trials
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