ArticleOncogene2016
Epigenetic modulation of a miR-296-5p:HMGA1 axis regulates Sox2 expression and glioblastoma stem cells.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
47 citing papers in PubMed, 75 citations in OpenAlex.
- Epigenetic silencing of miR-141 via core promoter methylation is associated with short-term bladder cancer progression.The Journal of biological chemistry · 2026Article
- HMGA proteins in the nervous system: role in brain tumorigenesis and neurodegeneration.Cell death discovery · 2026Review
- Telomeric Ends and Telomerase-Canonical and Non-Canonical Roles in Breast Cancer Tumorigenesis and Therapy Resistance.Biomedicines · 2026Review
- HMGA1 as a prognostic biomarker for gliomas: expression patterns, survival correlations, and clinical insights from a Pakistani cohort.Journal of neuro-oncology · 2025Article
- Multipronged SMAD pathway targeting by lipophilic poly(β-amino ester) miR-590-3p nanomiRs inhibits mesenchymal glioblastoma growth and prolongs survival.Signal transduction and targeted therapy · 2025Article
- Complicated crosstalk between HMGA and non-coding RNAs modulates hallmarks of cancer.Cancer cell international · 2025Review
- Hsa_circ_0000515 sequesters microRNA-296-5p and elevates RNF44 expression to encourage the NSCLC progression.Journal of cell communication and signaling · 2025Article
- Article
- Circulating Liquid Biopsy Biomarkers in Glioblastoma: Advances and Challenges.International journal of molecular sciences · 2024Review
- Morphological and Molecular Biological Characteristics of Experimental Rat Glioblastoma Tissue Strains Induced by Different Carcinogenic Chemicals.Biomedicines · 2024Article
- Advances in Diagnostic Tools and Therapeutic Approaches for Gliomas: A Comprehensive Review.Sensors (Basel, Switzerland) · 2023Review
- Systems Medicine for Precise Targeting of Glioblastoma.Molecular biotechnology · 2023Review
- Review
- Review
- Nucleic acid drug vectors for diagnosis and treatment of brain diseases.Signal transduction and targeted therapy · 2023Review
- Non-coding RNAs and glioma: Focus on cancer stem cells.Molecular therapy oncolytics · 2022Review
- Interplay of SOX transcription factors and microRNAs in the brain under physiological and pathological conditions.Neural regeneration research · 2022Review
- Sox2 induces glioblastoma cell stemness and tumor propagation by repressing TET2 and deregulating 5hmC and 5mC DNA modifications.Signal transduction and targeted therapy · 2022Article
- Exploring glioblastoma stem cell heterogeneity: Immune microenvironment modulation and therapeutic opportunities.Frontiers in oncology · 2022Review
- High Mobility Group A1 (HMGA1): Structure, Biological Function, and Therapeutic Potential.International journal of biological sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Solid malignancies contain subsets of multipotent cells that grow as spheres and efficiently propagate tumors in xenograft models, reflecting a stem-like, self-renewing and tumor-propagating phenotype. These cancer 'stem cells (SCs)' have been shown to maintain tumor growth, contribute to resistance and drive tumor recurrence. Cancer cell stemness is dynamically influenced by epigenetic mechanisms and differentially regulated coding and noncoding RNAs. How these mechanisms specifically contribute to the generation and/or maintenance of cancer SCs remains unclear. This study identifies a novel epigenetically regulated circuit that integrates microRNA, chromatin remodeling and the reprogramming transcription factor Sox2 to regulate glioblastoma (GBM)-propagating SCs. We show that miR-296-5p expression is repressed in a DNA methylation-dependent manner under conditions that promote GBM cell stemness and that miR-296-5p inhibits GBM cell stemness and their capacity to self-renew as spheres and propagate glioma xenografts in vivo. We show that the chromatin remodeling protein HMGA1 functions as a downstream effector of these biological responses to miR-296-5p and regulates Sox2 expression, a master driver of cell stemness, by modifying chromatin architecture at the Sox2 promoter. These results show for the first time that miR-296-5p inhibits transcriptional mechanisms that support GBM SCs and identify a miR-296-5p:HMGA1:Sox2 axis as a novel regulator of GBM SCs and candidate pathway for targeting therapies directed at depleting tumors of their tumor-propagating stem cell subsets.
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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.