ArticleInternational journal of clinical and experimental pathology2019
MiR-28-5p promotes human glioblastoma cell growth through inactivation of FOXO1.
Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The trial behind it
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Transposable Element-Derived miR-28-5p and miR-708-5p: Exploring Potential Roles in Lung Cancer.Non-coding RNA · 2025Article
- miR-28: A Tiny Player in Cancer Progression and Other Human Diseases.Biomolecules · 2025Review
- Transplantation of MiR-28-5p-Modified BMSCs Promotes Functional Recovery After Spinal Cord Injury.Molecular neurobiology · 2024Article
- Methods of miRNA delivery and possibilities of their application in neuro-oncology.Non-coding RNA research · 2023Review
- Forkhead box transcription factors (FOXOs and FOXM1) in glioma: from molecular mechanisms to therapeutics.Cancer cell international · 2023Review
- Article
- Specific microRNA Signature Kinetics inInternational journal of molecular sciences · 2023Article
- MicroRNA‑28‑3p inhibits angiotensin‑converting enzyme 2 ectodomain shedding in 293T cells treated with the spike protein of severe acute respiratory syndrome coronavirus 2 by targeting A disintegrin and metalloproteinase 17.International journal of molecular medicine · 2021Article
- MHC Class I Downregulation in Cancer: Underlying Mechanisms and Potential Targets for Cancer Immunotherapy.Cancers · 2020Review
- Association of the Epithelial-Mesenchymal Transition (EMT) with Cisplatin Resistance.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveGlioblastomais is one of the main universal, primary brain cancers, in adults, that has an extremely poor clinical prognosis and a median living period of 12-15 months, accounting for nearly 3-4% of all cancer-related deaths. MicroRNAs (miRNAs) play key roles in cancer pathogenesis by binding the specific and complementary sequences of the 3'UTR of target mRNAs to regulate protein synthesis. Therefore, recognizing functional miRNAs and the fundamental molecular mechanisms will offer novel evidences for the progress of targeted malignancy interferences. Our current study intended to explore the function of miR-28-5p in the promotion of the glioblastoma.
methodsHuman glioblastoma tissues, paired nearby normal/non-tumor tissues were accumulated from our hospital. Human glioblastoma SNB19 cells were infected by miR-28-5p mimics or miR-28-5p siRNA by lentivirus. Tumor spheres formation was used to evaluate the growth ability. MTT examine was applied for measuring viability. BrdU cell proliferation assay was applied to uncover the proliferation ability of SNB19 glioblastoma cells. Real-time PCR was conducted to identify miRNA expression. Western blot analysis was employed to measure protein expression. Dual-luciferase FOXO1-3'UTR reporter was used to determine the ability of miR-28-5p to regulate FOXO1.
resultsExpression of miR-28-5p was explored to be increased in both human glioblastoma tissues and cell lines. Up-regulated miR-28-5p expression promotes tumor spheres formation, cell viability, and proliferation ability of glioblastoma cells. FOXO1 was found to be the target of miR-28-5p and the activity of FOXO1 was down-regulated by miR-28-5p in glioblastoma cells.
conclusionsMiR-28-5p is an oncogene and promotes the occurrence of glioblastoma by directly targeting the FOXO1.
Indexed as
Identifiers
31934134PMC6949703W3004760363What 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.