ArticleIn vitro cellular & developmental biology. Animal2013
MicroRNA-125b inhibitor sensitizes human primary glioblastoma cells to chemotherapeutic drug temozolomide on invasion.
Article in In vitro cellular & developmental biology. Animal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- MicroRNAs as the pivotal regulators of Temozolomide resistance in glioblastoma.Molecular brain · 2024Review
- The functional mechanism of miR-125b in gastric cancer and its effect on the chemosensitivity of cisplatin.Oncotarget · 2018Article
- MiR-29b inhibits the growth of glioma via MYCN dependent way.Oncotarget · 2017Article
- Demethoxycurcumin was superior to temozolomide in the inhibition of the growth of glioblastoma stem cells in vivo.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- PI3K inhibitor combined with miR-125b inhibitor sensitize TMZ-induced anti-glioma stem cancer effects through inactivation of Wnt/β-catenin signaling pathway.In vitro cellular & developmental biology. Animal · 2015Article
- Regulation of expression of O6-methylguanine-DNA methyltransferase and the treatment of glioblastoma (Review).International journal of oncology · 2015Review
- Decreased Expression of miR-15b in Human Gliomas is Associated with Poor Prognosis.Cancer biotherapy & radiopharmaceuticals · 2015Article
- MicroRNA expression signatures and their correlation with clinicopathological features in glioblastoma multiforme.Neuromolecular medicine · 2014Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant gliomas are treated with a combination of surgery, radiation, and temozolomide (TMZ), but these therapies ultimately fail due to tumor recurrence. In this study, we aimed to identify the combined effects of miR-125b and TMZ involved in the invasive pathogenesis of glioblastoma cells. The effects of miR-125b and TMZ on cell invasion were analyzed by Transwell assays. Unexpectedly, either overexpression or downregulation of miR-125b has no function on glioblastoma cell invasion. However, knockdown of miR-125b could enhance the effects of TMZ on glioblastoma cell invasion. Conversely, overexpression of miR-125b could decrease such effects of TMZ. Further research on the mechanism demonstrated that such function of miR-125b knockdown on enhancing the effects of TMZ was involved in downregulation of Notch1. Notch1 was overexpressed in glioblastoma cells, and found by us that downregulation of Notch1 expression decreased the cell invasion of glioblastoma cells. Knockdown of miR-125b combined with TMZ enhancely downregulated Notch1 and inhibited cell invasion of malignant glioblastoma. These findings indicate that the combination of miR-125b inhibitor and TMZ treatment could effectively inhibit the glioblastoma cell invasion by inhibiting Notch1 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.