ArticleJournal of neuro-oncology2017
MiR-181b modulates chemosensitivity of glioblastoma multiforme cells to temozolomide by targeting the epidermal growth factor receptor.
Article in Journal of neuro-oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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
17 citing papers in PubMed, 31 citations in OpenAlex.
- Unraveling the mechanisms of glioblastoma's resistance: investigating the influence of tumor suppressor p53 and non-coding RNAs.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Role of Non-coding RNAs in the Response of Glioblastoma to Temozolomide.Molecular neurobiology · 2025Review
- MicroRNAs as the pivotal regulators of Temozolomide resistance in glioblastoma.Molecular brain · 2024Review
- miRNAs and related genetic biomarkers according to the WHO glioma classification: From diagnosis to future therapeutic targets.Non-coding RNA research · 2024Review
- Zinc Finger E-Box Binding Homeobox Family: Non-Coding RNA and Epigenetic Regulation in Gliomas.Biomedicines · 2023Review
- A rationally identified panel of microRNAs targets multiple oncogenic pathways to enhance chemotherapeutic effects in glioblastoma models.Scientific reports · 2022Article
- Review
- Functions of non-coding RNAs in regulating cancer drug targets.Acta biochimica et biophysica Sinica · 2022Review
- The genotypic and phenotypic impact of hypoxia microenvironment on glioblastoma cell lines.BMC cancer · 2021Article
- Article
- Functions and clinical significance of circular RNAs in glioma.Molecular cancer · 2020Review
- MiR-181b suppress glioblastoma multiforme growth through inhibition of SP1-mediated glucose metabolism.Cancer cell international · 2020Article
- MicroRNA based theranostics for brain cancer: basic principles.Journal of experimental & clinical cancer research : CR · 2019Review
- Oligonucleotide Therapeutics as a New Class of Drugs for Malignant Brain Tumors: Targeting mRNAs, Regulatory RNAs, Mutations, Combinations, and Beyond.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- IGF-1-enhanced miR-513a-5p signaling desensitizes glioma cells to temozolomide by targeting the NEDD4L-inhibited Wnt/β-catenin pathway.PloS one · 2019Article
- Aberrant miRNAs Regulate the Biological Hallmarks of Glioblastoma.Neuromolecular medicine · 2018Review
- miR-1268a regulates ABCC1 expression to mediate temozolomide resistance in glioblastoma.Journal of neuro-oncology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Temozolomide (TMZ) is a promising chemotherapeutic agent to treat Glioblastoma multiforme (GBM). However, resistance to TMZ develops quickly with a high frequency. The mechanisms underlying GBM cells' resistance to TMZ are not fully understood. MicroRNAs (miRNAs) are small, non-coding RNA molecules that regulate protein expression by cleaving or repressing the translation of target mRNAs. Recently, miRNAs have been discovered to play important roles in drug resistance. A previous study showed that miR-181b in involved in glioma tumorigenesis. Thus, it would be valuable to explore the functions and mechanisms of miR-181b in regulating GMB cells' sensitivity to TMZ. In this study, quantitative real-time reverse transcription PCR (qRT-PCR) data indicated that miR-181b was significantly downregulated in recurrent GBM tissues compared with initial GBM tissues. We also found that miR-181b overexpression increased the chemo-sensitivity of GBM cells to TMZ and potentiated TMZ-induced apoptosis in vitro and in vivo. Moreover, we demonstrated that the epidermal growth factor receptor (EGFR) was a direct target of miR-181b: restoration of EGFR rescued the inhibitory effects of miR-181b and TMZ treatment. Taken together, our data support strongly an important role for miR-181b in conferring TMZ resistance by targeting EGFR expression.
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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.