ArticleBMC cancer2014
MiR-181b sensitizes glioma cells to teniposide by targeting MDM2.
Article in BMC cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 62 citations in OpenAlex.
- MDM2 provides TOP2 poison resistance by promoting proteolysis of TOP2βcc in a p53-independent manner.Cell death & disease · 2024Article
- Upregulating miR-181b promotes ferroptosis in osteoarthritic chondrocytes by inhibiting SLC7A11.BMC musculoskeletal disorders · 2023Article
- Therapeutic and Diagnostic Potential of Exosomes as Drug Delivery Systems in Brain Cancer.Pharmaceutics · 2023Review
- Regulation of topoisomerase II stability and activity by ubiquitination and SUMOylation: clinical implications for cancer chemotherapy.Molecular biology reports · 2021Review
- Exosomes as New Biomarkers and Drug Delivery Tools for the Prevention and Treatment of Various Diseases: Current Perspectives.International journal of molecular sciences · 2021Review
- Emerging Roles and Potential Applications of Non-Coding RNAs in Glioblastoma.International journal of molecular sciences · 2020Review
- MicroRNA-585 inhibits human glioma cell proliferation by directly targeting MDM2.Cancer cell international · 2020Article
- Advancing towards Effective Glioma Therapy: MicroRNA Derived from Umbilical Cord Mesenchymal Stem Cells' Extracellular Vesicles.The Malaysian journal of medical sciences : MJMS · 2019Review
- Review
- Article
- miR-181a/b therapy in lung cancer: reality or myth?Molecular oncology · 2019Review
- Non-Coding RNAs in Glioma.Cancers · 2018Review
- Aberrant miRNAs Regulate the Biological Hallmarks of Glioblastoma.Neuromolecular medicine · 2018Review
- miR-181b inhibits chemoresistance in cisplatin-resistant H446 small cell lung cancer cells by targeting Bcl-2.Archives of medical science : AMS · 2018Article
- miR-197 is downregulated in cervical carcinogenesis and suppresses cell proliferation and invasion through targeting forkhead box M1.Oncology letters · 2018Article
- Review
- Evaluation of apoptosis induced by exposure to antineoplastic drugs in peripheral blood lymphocytes of nurses.Molecular medicine reports · 2017Article
- RNA interference for glioblastoma therapy: Innovation ladder from the bench to clinical trials.Life sciences · 2017Review
- MiR-181b modulates EGFR-dependent VCAM-1 expression and monocyte adhesion in glioblastoma.Oncogene · 2017Article
- MicroRNA-181b Inhibits Cellular Proliferation and Invasion of Glioma Cells via Targeting Sal-Like Protein 4.Oncology research · 2017Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough the incidence of glioma is relatively low, it is the most malignant tumor of the central nervous system. The prognosis of high-grade glioma patient is very poor due to the difficulties in complete resection and resistance to radio-/chemotherapy. Therefore, it is worth investigating the molecular mechanisms involved in glioma drug resistance. MicroRNAs have been found to play important roles in tumor progression and drug resistance. Our previous work showed that miR-181b is involved in the regulation of temozolomide resistance. In the current study, we investigated whether miR-181b also plays a role in antagonizing the effect of teniposide.
methodsMiR-181b expression was measured in 90 glioma patient tissues and its relationship to prognosis of these patients was analyzed. Cell sensitivity to teniposide was tested in 48 primary cultured glioma samples. Then miR-181b stably overexpressed U87 cells were generated. The candidate genes of miR-181b from our previous study were reanalyzed, and the interaction between miR-181b and target gene MDM2 was confirmed by dual luciferase assay. Cell sensitivity to teniposide was detected on miR-181b over expressed and MDM2 down regulated cells.
resultsOur data confirmed the low expression levels of miR-181b in high-grade glioma tissues, which is related to teniposide resistance in primary cultured glioma cells. Overexpression of miR-181b increased glioma cell sensitivity to teniposide. Through target gene prediction, we found that MDM2 is a candidate target of miR-181b. MDM2 knockdown mimicked the sensitization effect of miR-181b. Further study revealed that miR-181b binds to the 3'-UTR region of MDM2 leading to the decrease in MDM2 levels and subsequent increase in teniposide sensitivity. Partial restoration of MDM2 attenuated the sensitivity enhancement by miR-181b.
conclusionsMiR-181b is an important positive regulator on glioma cell sensitivity to teniposide. It confers glioma cell sensitivity to teniposide through binding to the 3'-UTR region of MDM2 leading to its reduced expression. Our findings not only reveal the novel mechanism involved in teniposide resistance, but also shed light on the optimization of glioma treatment in the future.
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