ArticleOncoTargets and therapy2020
MicroRNA-6071 Suppresses Glioblastoma Progression Through the Inhibition of PI3K/AKT/mTOR Pathway by Binding to ULBP2.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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
11 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- lncDILC Downregulation in Liver Cancer-Associated Fibroblasts Drives Pro-Invasive Conversion via a miR-6071-ZNF395 Axis.Cancer science · 2026Article
- Emerging Insights into the PI3K/AKT/mTOR Signaling Pathway and Non-Coding RNA-mediated Drug Resistance in Glioblastoma.Current molecular medicine · 2025Review
- A novel immune score model predicting the prognosis and immunotherapy response of breast cancer.Scientific reports · 2023Article
- Significance of logistic regression scoring model based on natural killer cell-mediated cytotoxic pathway in the diagnosis of colon cancer.Frontiers in immunology · 2023Article
- Signatures of genetic variation in human microRNAs point to processes of positive selection and population-specific disease risks.Human genetics · 2022Article
- METTL7B contributes to the malignant progression of glioblastoma by inhibiting EGR1 expression.Metabolic brain disease · 2022Article
- Hypoxia-Driven M2-Polarized Macrophages Facilitate Cancer Aggressiveness and Temozolomide Resistance in Glioblastoma.Oxidative medicine and cellular longevity · 2022Article
- The Role of Micro RNAs in Regulating PI3K/AKT Signaling Pathways in Glioblastoma.Iranian journal of pathology · 2022Review
- Article
- BASP1 Suppresses Cell Growth and Metastasis through Inhibiting Wnt/BioMed research international · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe purpose of this study was to explore the effect of microRNA-6071 (miR-6071) on glioblastoma (GBM) and its potential mechanisms.
methodsIn this study, the expressions of miR-6071 and UL16 binding protein 2 (ULBP2) were measured by qRT-RCR in GBM tissues and cells. The prognostic values of miR-6071 and ULBP2 were evaluated by Kaplan-Meier methods using the data obtained from The Cancer Genome Atlas (TCGA) database. The cell clones, proliferation, apoptosis, migration and invasion in GBM cells were detected by colony formation assay, EdU assay, flow cytometry, wound-healing assay and transwell assay. The targeting relationship between miR-6071 and ULBP2 was predicted by Targetscan 7.2 and further verified by dual-luciferase reporter gene assay. Moreover, the expressions of Bax, caspase-3, Bcl-2, matrix metalloproteinases 2 (MMP-2), MMP-9, phosphatidylinositol 3'-kinase (PI3K), p-PI3K, protein kinase B (AKT), p-AKT, mammalian target of rapamycin (mTOR) and p-mTOR were measured by Western blot.
resultsmiR-6071 was lowly expressed and ULBP2 was highly expressed in GBM tissues and cells. miR-6071 significantly repressed the proliferation, migration and invasion, and promoted apoptosis in GBM cells. Moreover, miR-6071 also inhibited the activation of PI3K/AKT/mTOR pathway in GBM cells. Additionally, miR-6071 has been shown to negatively regulate ULBP2 expression. We also confirmed that ULBP2 could reverse the effects of miR-6071 on GBM cells through regulating PI3K/AKT/mTOR pathway.
conclusionOur study demonstrated that miR-6071 could suppress cell proliferation, migration and invasion, as well as promote apoptosis through the inhibition of PI3K/Akt/mTOR pathway by binding to ULBP2 in GBM.
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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.