ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
MiR-338-5p sensitizes glioblastoma cells to radiation through regulation of genes involved in DNA damage response.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Diagnostic significance and potential function of miR-338-5p in hepatocellular carcinoma: A bioinformatics study with microarray and RNA sequencing data.Molecular medicine reports · 2018Pooled it
- The role of abnormal epigenetic regulation of small GTPases in glioma (Review).International journal of oncology · 2025Review
- Nucleic acid immunotherapeutics and vaccines: A promising approach to glioblastoma multiforme treatment.International journal of pharmaceutics · 2023Review
- Glioblastoma and cerebral organoids: development and analysis of an in vitro model for glioblastoma migration.Molecular oncology · 2023Article
- Biased holoenzyme assembly of protein phosphatase 2A (PP2A): From cancer to small molecules.The Journal of biological chemistry · 2022Review
- MicroRNAs as prognostic markers and therapeutic targets in gliomas.Non-coding RNA research · 2022Review
- Article
- Deciphering specific miRNAs in brain tumors: a 5-miRNA signature in glioblastoma.Molecular genetics and genomics : MGG · 2022Article
- Footprints of microRNAs in Cancer Biology.Biomedicines · 2021Review
- Phosphatidylinositol 3,4,5-Trisphosphate-Dependent Rac Exchanger 2 Protein Facilitates Glioma Progression via Akt and Stat3 Signaling.Journal of molecular neuroscience : MN · 2021Article
- Article
- Molecular interactions of miR-338 during tumor progression and metastasis.Cellular & molecular biology letters · 2021Review
- Glioblastoma and MiRNAs.Cancers · 2021Review
- ComprehensiveFrontiers in oncology · 2021Article
- The Emerging Roles of RNA Modifications in Glioblastoma.Cancers · 2020Review
- MicroRNA-338-5p reverses chemoresistance and inhibits invasion of esophageal squamous cell carcinoma cells by targeting Id-1.Cancer science · 2019Article
- Hypoxia Induces Drug Resistance in Colorectal Cancer through the HIF-1α/miR-338-5p/IL-6 Feedback Loop.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- The CTIP-mediated repair of TNF-α-induced DNA double-strand break was impaired by miR-130b in cervical cancer cell.Cell biochemistry and function · 2019Article
- Analysis of microarray data for identification of key microRNA signatures in glioblastoma multiforme.Oncology letters · 2019Article
- MiR-338-5p promotes metastasis of colorectal cancer by inhibition of phosphatidylinositol 3-kinase, catalytic subunit type 3-mediated autophagy pathway.EBioMedicine · 2019Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is the most aggressive form of brain tumor. Despite radical surgery and radiotherapy supported by chemotherapy, the disease still remains incurable with an extremely low median survival rate of 12-15 months from the time of initial diagnosis. The main cause of treatment failure is considered to be the presence of cells that are resistant to the treatment. MicroRNAs (miRNAs) as regulators of gene expression are involved in the tumor pathogenesis, including GBM. MiR-338 is a brain-specific miRNA which has been described to target pathways involved in proliferation and differentiation. In our study, miR-338-3p and miR-338-5p were differentially expressed in GBM tissue in comparison to non-tumor brain tissue. Overexpression of miR-338-3p with miRNA mimic did not show any changes in proliferation rates in GBM cell lines (A172, T98G, U87MG). On the other hand, pre-miR-338-5p notably decreased proliferation and caused cell cycle arrest. Since radiation is currently the main treatment modality in GBM, we combined overexpression of pre-miR-338-5p with radiation, which led to significantly decreased cell proliferation, increased cell cycle arrest, and apoptosis in comparison to irradiation-only cells. To better elucidate the mechanism of action, we performed gene expression profiling analysis that revealed targets of miR-338-5p being Ndfip1, Rheb, and ppp2R5a. These genes have been described to be involved in DNA damage response, proliferation, and cell cycle regulation. To our knowledge, this is the first study to describe the role of miR-338-5p in GBM and its potential to improve the sensitivity of GBM to radiation.
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Registered trials
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