ArticleGenes2023
Enhancing Transcriptional Reprogramming of Mesenchymal Glioblastoma with Grainyhead-like 2 and HDAC Inhibitors Leads to Apoptosis and Cell-Cycle Dysregulation.
Article in Genes, 2023. 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, 6 citations in OpenAlex.
- Targeting glioblastoma with HDAC inhibitors: insights into hydroxamic acid-based therapeutic strategies.Acta neuropathologica communications · 2025Article
- Cytokine and epigenetic regulation of CEACAM6 mediates EGFR-driven signaling and drug response in lung adenocarcinoma.NPJ precision oncology · 2025Article
- SNAI2 cooperates with MEK1/2 and HDACs to suppress BIM- and BMF-dependent apoptosis in TERT promoter mutant cancers.PloS one · 2025Article
- PRIM2: A Marker of MYC-driven Hyper-proliferation, Disease Progression, Tumor Aggressiveness and Poor Survival in Glioma Patients.Cancer genomics & proteomicsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) tumor cells exhibit mesenchymal properties which are thought to play significant roles in therapeutic resistance and tumor recurrence. An important question is whether impairment of the mesenchymal state of GBM can sensitize these tumors to therapeutic intervention. HDAC inhibitors (HDACi) are being tested in GBM for their ability promote mesenchymal-to-epithelial transcriptional (MET) reprogramming, and for their cancer-specific ability to dysregulate the cell cycle and induce apoptosis. We set out to enhance the transcriptional reprogramming and apoptotic effects of HDACi in GBM by introducing an epithelial transcription factor, Grainyhead-like 2 (GRHL2), to specifically counter the mesenchymal state. GRHL2 significantly enhanced HDACi-mediated MET reprogramming. Surprisingly, we found that inducing GRHL2 in glioma stem cells (GSCs) altered cell-cycle drivers and promoted aneuploidy. Mass spectrometry analysis of GRHL2 interacting proteins revealed association with several key mitotic factors, suggesting their exogenous expression disrupted the established mitotic program in GBM. Associated with this cell-cycle dysregulation, the combination of GRHL2 and HDACi induced elevated levels of apoptosis. The key implication of our study is that although genetic strategies to repress the mesenchymal properties of glioblastoma may be effective, biological interactions of epithelial factors in mesenchymal cancer cells may dysregulate normal homeostatic cellular mechanisms.
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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.