ArticleOncotarget2016
miR128-1 inhibits the growth of glioblastoma multiforme and glioma stem-like cells via targeting BMI1 and E2F3.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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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
40 citing papers in PubMed, 73 citations in OpenAlex.
- Review
- Insights Into the Role of Bmi-1 Deregulation in Promoting Stemness and Therapy Resistance in Glioblastoma: A Narrative Review.Cancer medicine · 2025Review
- MiR-128-3p - a gray eminence of the human central nervous system.Molecular therapy. Nucleic acids · 2024Review
- Glioblastoma Therapy: Past, Present and Future.International journal of molecular sciences · 2024Review
- Use of microRNAs as Diagnostic, Prognostic, and Therapeutic Tools for Glioblastoma.International journal of molecular sciences · 2024Review
- Exploring the Role of microRNAs in Glioma Progression, Prognosis, and Therapeutic Strategies.Cancers · 2023Review
- ADAMTS9-AS1 Long Non‑coding RNA Sponges miR‑128 and miR-150 to Regulate Ras/MAPK Signaling Pathway in Glioma.Cellular and molecular neurobiology · 2023Article
- MicroRNAs as Targets for Cancer Diagnosis: Interests and Limitations.Advanced pharmaceutical bulletin · 2023Review
- Review
- microRNAs (miRNAs) in Glioblastoma Multiforme (GBM)-Recent Literature Review.International journal of molecular sciences · 2023Review
- Non-coding RNAs and glioma: Focus on cancer stem cells.Molecular therapy oncolytics · 2022Review
- A tumor microenvironment-responsive micelle co-delivered radiosensitizer Dbait and doxorubicin for the collaborative chemo-radiotherapy of glioblastoma.Drug delivery · 2022Article
- LINC02381-ceRNA exerts its oncogenic effect through regulation of IGF1R signaling pathway in glioma.Journal of neuro-oncology · 2022Article
- Advances in Polyhydroxyalkanoate Nanocarriers for Effective Drug Delivery: An Overview and Challenges.Nanomaterials (Basel, Switzerland) · 2022Review
- CircLATS2 Regulates miR-520a-3p/E2F7/p-VEGFR2 Signaling Pathway to Promote Hepatocellular Carcinoma Progression and Angiogenesis.Journal of oncology · 2022Article
- miRNA-200c-3p targets talin-1 to regulate integrin-mediated cell adhesion.Scientific reports · 2021Article
- Combined BRM270 and endostatin inhibit relapse of NSCLC while suppressing lung cancer stem cell proliferation induced by endostatin.Molecular therapy oncolytics · 2021Article
- Role of microRNAs in glioblastoma.Oncotarget · 2021Article
- Expression analysis of progesterone‑regulated miRNAs in cells derived from human glioblastoma.Molecular medicine reports · 2021Article
- CircAGAP1 promotes tumor progression by sponging miR-15-5p in clear cell renal cell carcinoma.Journal of experimental & clinical cancer research : CR · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA128-1 (miR128-1), as a brain-specific miRNA, is downregulated in glioblastoma multiforme (GBM) and closely associated with the progression of GBM. However, the underlying molecular mechanism of the downregulation and its role in the regulation of tumorigenesis and anticancer drug resistance in GBM remains largely unknown. In the current study,we found that miR128-1 was downregulated in GBM and glioma stem-like cells (GSCs). Intriguingly, treatment with the DNA methylation inhibitors 5-Aza-CdR (Aza) and 4-phenylbutyric acid (PBA) resulted in miR128-1 upregulation in both GBM cells and GSCs. Either forced expression of miR128-1 or Aza/PBA treatment inhibited tumor cell proliferation, migration and invasion in vitro. Moreover, overexpression of miR128-1 inhibited the growth of transplant tumor in vivo. BMI1 and E2F3 were found to be direct targets of miR128-1 and downregulated by miR128-1 in vitro and in vivo. Our results revealed a mechanism of methylation that controls miR128-1 expression in GBM cells and GSCs and indicate miR128-1 could function as a tumor suppressor in GBM by negatively regulating tumor cell proliferation, invasion and self-renewal through direct targeting BMI1 and E2F3. Our findings suggest that DNA methylation inhibitors are potential agents for GBM treatment by upregulating miR-128-1.
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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.