ArticleScientific reports2017
HCMV-encoded miR-UL112-3p promotes glioblastoma progression via tumour suppressor candidate 3.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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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, 25 citations in OpenAlex.
- Targeting Human Cytomegalovirus as a Novel Approach for Glioblastoma Treatment.Pathogens (Basel, Switzerland) · 2025Review
- Role of cytomegalovirus in glioblastoma development: promoter or culprit?Virology journal · 2025Review
- miRNAs: Targets to Investigate Herpesvirus Infection Associated with Neurological Disorders.International journal of molecular sciences · 2023Review
- Review
- Human cytomegalovirus-encoded microRNAs expression profile in plasma of patients with aortic dissection.Journal of cardiothoracic surgery · 2023Article
- HCMV-miR-US33-5p promotes apoptosis of aortic vascular smooth muscle cells by targeting EPAS1/SLC3A2 pathway.Cellular & molecular biology letters · 2022Article
- The Emerging Role of Non-Coding RNAs in the Regulation of Virus Replication and Resultant Cellular Pathologies.International journal of molecular sciences · 2022Review
- Mechanisms of Survival of Cytomegalovirus-Infected Tumor Cells.Molecular biology · 2022Article
- Human Cytomegalovirus Induced Aberrant Expression of Non-coding RNAs.Frontiers in microbiology · 2022Review
- Human cytomegalovirus (HCMV)-encoded microRNAs: potential biomarkers and clinical applications.RNA biology · 2021Review
- Review
- Efficacy of small-dose ganciclovir on cytomegalovirus infections in children and its effects on liver function and miR-UL112-3p expression.Experimental and therapeutic medicine · 2021Article
- Apoptosis Disorder, a Key Pathogenesis of HCMV-Related Diseases.International journal of molecular sciences · 2021Review
- Regulation of Latency and Reactivation by Human Cytomegalovirus miRNAs.Pathogens (Basel, Switzerland) · 2021Review
- Immune Landscape of CMV Infection in Cancer Patients: From "Canonical" Diseases Toward Virus-Elicited Oncomodulation.Frontiers in immunology · 2021Review
- Levels of human cytomegalovirus miR-US25-1-5p and miR-UL112-3p in serum extracellular vesicles from infants with HCMV active infection are significantly correlated with liver damage.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2020Article
- Low levels of tumor suppressor candidate 3 predict poor prognosis of patients with hepatocellular carcinoma.OncoTargets and therapy · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most prevalent and lethal type of primary malignant brain tumour. Recent studies suggest that the discovery of human cytomegalovirus (HCMV)-encoded microRNAs (miRNAs) might play a role in the pathogenesis of diseases, including GBM. In this study, we aimed to analyse the expression and function of HCMV-encoded miRNAs in GBM. We found that miR-UL112-3p expression was significantly elevated in GBM, and its expression levels were highly associated with glioma size, differentiation, WHO stage and the overall and disease-free survival of patients. The overexpression of miR-UL112-3p in the GBM cells promoted cell proliferation, clone formation, migration and invasion. In contrast, the down-regulation of miR-UL112-3p exerted an inverse effects. Tumour suppressor candidate 3 (TUSC3), a potential target gene of miR-UL112-3p, was inversely correlated with miR-UL112-3p expression in GBM tissues and cell lines. Furthermore, we demonstrated that TUSC3 was directly regulated by miR-UL112-3p, and the ectopic expression of TUSC3 reversed the effects of miR-UL112-3p on GBM progression via the AKT signalling pathway. Taken together, these findings collectively demonstrate that miR-UL112-3p exerts its oncogene function by directly targeting TUSC3 in GBM, indicating a potential novel therapeutic target for 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.