ArticleScience signaling2015
Feedback circuitry between miR-218 repression and RTK activation in glioblastoma.
Article in Science signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Glycoprotein NMB mediates bidirectional GSC-TAM interactions to promote tumor progression.JCI insight · 2025Article
- Discovery of miRNA-mRNA regulatory networks in glioblastoma reveals novel insights into tumor microenvironment remodeling.Scientific reports · 2024Article
- Role of STAT3 in cancer cell epithelial‑mesenchymal transition (Review).International journal of oncology · 2024Review
- Spatial distribution and functional relevance of FGFR1 and FGFR2 expression for glioblastoma tumor invasion.Cancer letters · 2023Article
- Tumor suppressor miR-218 directly targets epidermal growth factor receptor (EGFR) expression in triple-negative breast cancer, sensitizing cells to irradiation.Journal of cancer research and clinical oncology · 2023Article
- Review
- A rationally identified panel of microRNAs targets multiple oncogenic pathways to enhance chemotherapeutic effects in glioblastoma models.Scientific reports · 2022Article
- miR-218 affects the ECM composition and cell biomechanical properties of glioblastoma cells.Journal of cellular and molecular medicine · 2022Article
- Noncoding RNAs involved in the STAT3 pathway in glioma.Cancer cell international · 2021Review
- Aberrant expression of RSK1 characterizes high-grade gliomas with immune infiltration.Molecular oncology · 2020Article
- Systems and Synthetic microRNA Biology: From Biogenesis to Disease Pathogenesis.International journal of molecular sciences · 2019Review
- Aberrant miRNAs Regulate the Biological Hallmarks of Glioblastoma.Neuromolecular medicine · 2018Review
- Review
- The EGLN-HIF OMolecular cell · 2017Review
- MNK Inhibition Disrupts Mesenchymal Glioma Stem Cells and Prolongs Survival in a Mouse Model of Glioblastoma.Molecular cancer research : MCR · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Receptor tyrosine kinase (RTK) signaling promotes the growth and progression of glioblastoma (GBM), a highly aggressive type of brain tumor. We previously reported that decreased miR-218 expression in GBM directly promotes RTK activity by increasing the expression of key RTKs and their signaling mediators, including the RTK epidermal growth factor receptor (EGFR), phospholipase C-γ1 (PLCγ1), and the kinases PIK3CA and ARAF. However, increased RTK signaling usually activates negative feedback mechanisms to maintain homeostasis. We found that decreased miR-218 expression in GBM cells also increased the expression of genes encoding additional upstream and downstream components of RTK signaling pathways, including the RTK platelet-derived growth factor receptor α (PDGFRα) and the kinases ribosomal S6 kinase 2 (RSK2) and S6 kinase 1 (S6K1), that collectively overrode the negative feedback mechanism. Furthermore, increased RTK signaling itself suppressed miR-218 expression. Mass spectrometry and DNA pull-down identified binding of signal transducer and activator of transcription 3 (STAT3) along with the transcriptional repressor BCL2-associated transcription factor 1 (BCLAF1) directly to the miR-218 locus. These data identify previously unknown feedback loops by which miR-218 repression promotes increased RTK signaling in high-grade gliomas.
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What OpenQuestion holds
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.