ArticleMolecular oncology2021
Downregulation of miR-326 and its host gene β-arrestin1 induces pro-survival activity of E2F1 and promotes medulloblastoma growth.
Article in Molecular oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 12 citations in OpenAlex.
- CD133 structural instability as a gateway to medulloblastoma vulnerability.Cancer cell international · 2026Article
- Exploration of miR-326 delivery via biocompatible polymeric nanoparticles in medulloblastoma: A preliminary study.Molecular therapy. Nucleic acids · 2026Article
- Gut Microbiota-induced Long Non-coding RNA Snhg9 Regulates the Development of Human Malignant Tumors.Current molecular medicine · 2026Review
- MiR-326: Role and significance in brain cancers.Non-coding RNA research · 2025Review
- Circulating lncRNA HOTAIR is a biomarker for pediatric acute lymphoblastic leukemia and mediator of miR-326 exosomal export.Scientific reports · 2025Article
- MiRNAs as major players in brain health and disease: current knowledge and future perspectives.Cell death discovery · 2025Review
- MAFG-DT promotes prostate cancer bone metastasis through activation of the Wnt/β-catenin pathway.Frontiers in oncology · 2024Article
- Crosstalk between Noncoding RNAs and the Epigenetics Machinery in Pediatric Tumors and Their Microenvironment.Cancers · 2023Review
- Nanoparticles for Drug and Gene Delivery in Pediatric Brain Tumors' Cancer Stem Cells: Current Knowledge and Future Perspectives.Pharmaceutics · 2023Review
- β-arrestin1-E2F1-ac axis regulates physiological apoptosis and cell cycle exit in cellular models of early postnatal cerebellum.Frontiers in cell and developmental biology · 2023Article
- The long and short non-coding RNAs modulating EZH2 signaling in cancer.Journal of hematology & oncology · 2022Review
- Long noncoding RNA FAM225A promotes the malignant progression of gastric cancer through the miR-326/PADI2 axis.Cell death discovery · 2022Article
- Splice and Dice: Intronic microRNAs, Splicing and Cancer.Biomedicines · 2021Review
- Epigenetic modulators for brain cancer stem cells: Implications for anticancer treatment.World journal of stem cells · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistent mortality rates of medulloblastoma (MB) and severe side effects of the current therapies require the definition of the molecular mechanisms that contribute to tumor progression. Using cultured MB cancer stem cells and xenograft tumors generated in mice, we show that low expression of miR-326 and its host gene β-arrestin1 (ARRB1) promotes tumor growth enhancing the E2F1 pro-survival function. Our models revealed that miR-326 and ARRB1 are controlled by a bivalent domain, since the H3K27me3 repressive mark is found at their regulatory region together with the activation-associated H3K4me3 mark. High levels of EZH2, a feature of MB, are responsible for the presence of H3K27me3. Ectopic expression of miR-326 and ARRB1 provides hints into how their low levels regulate E2F1 activity. MiR-326 targets E2F1 mRNA, thereby reducing its protein levels; ARRB1, triggering E2F1 acetylation, reverses its function into pro-apoptotic activity. Similar to miR-326 and ARRB1 overexpression, we also show that EZH2 inhibition restores miR-326/ARRB1 expression, limiting E2F1 pro-proliferative activity. Our results reveal a new regulatory molecular axis critical for MB progression.
Indexed as
Identifiers
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.