ReviewCells2025
Similarities in Mechanisms of Ovarian Cancer Metastasis and Brain Glioblastoma Multiforme Invasion Suggest Common Therapeutic Targets.
Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Current Research on the Control Mechanisms of Cell Survival and Proliferation as Potential Interaction Sites with Pentacyclic Triterpenoids in Ovarian Cancer.International journal of molecular sciences · 2025Review
- Curcumin-Induced Molecular Mechanisms in U-87 MG Glioblastoma Cells: Insights from Global Gene Expression Profiling.Molecules (Basel, Switzerland) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-to-mesenchymal transition (EMT) is a critical process in malignant ovarian cancer metastasis. EMT involves the conversion of epithelial cells to mesenchymal cells, conferring enhanced migratory and invasive capabilities. Glioblastoma multiforme (GBM) is the most common malignant primary brain tumor and exhibits an aggressive invasive phenotype that mimics some steps of EMT but does not undergo true metastasis, i.e., the invasion of other organ systems. This study conducts a comparative genomic analysis of EMT in ovarian cancer and invasion in GBM-two malignancies characterized by poor prognosis and limited therapies. Investigating the molecular biology in ovarian cancer and GBM demonstrates shared mechanisms of tumor progression, such as similar genetic and molecular pathways influencing cell plasticity, invasion, and resistance to therapy. The comparative analysis reveals commonalities and differences in the regulatory networks and gene expression profiles associated with EMT and invasion in these cancers. Key findings include the identification of core EMT regulators, such as TWIST1, SNAIL, and ZEB1, which are upregulated in both ovarian cancer and GBM, promoting mesenchymal phenotypes and metastasis. Additionally, the analysis uncovers EMT-related pathways, such as the PI3K/AKT and TGF-β signaling, which are critical in both cancers but exhibit distinct regulatory dynamics. Understanding the intricacies of EMT in ovarian cancer and invasion in GBM provides valuable insights into their aggressive behavior and identifies potential common therapeutic targets. The findings stress the importance of targeting EMT/invasion transitions to develop effective treatments to halt progression and improve patient outcomes in these malignancies.
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Registered trials
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