Evidence map›Paper›PMID 40688500›Full record

ArticleBiochemistry and biophysics reports2025

Exploring LAT-derived miRNAs as regulatory agents of EphrinA3 in glioblastoma multiforme.

Fatemeh Saadatpour, Ehsan Arefian

Abstract read
In one paragraph

Article in Biochemistry and biophysics reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Fatemeh SaadatpourMolecular Virology Lab, Department of Microbiology, School of Biology, College of Science, University of Tehran, Tehran, Iran.
Ehsan ArefianMolecular Virology Lab, Department of Microbiology, School of Biology, College of Science, University of Tehran, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: This study focuses on the findings related to Latency- Associated Transcript (LAT)- derived miRNAs and their interactions with ephrin family genes, especially Method: The differential expression of the Ephrin (EFN) family in GBM was analyzed using TCGA and GEO databases, alongside survival data from the Kaplan-Meier Plotter. Bioinformatics predicted LAT-derived miRNAs targeting EFN genes, which were validated in vitro. Luciferase assays confirmed miR-H2 and miR-H3's targeting of Results: EphrinA3 is significantly overexpressed in GBM tissues, and its expression level is correlated with the prognosis of GBM patients. Both miR-H2-3p and miR-H3-3p effectively target EphrinA3, resulting in approximately a twofold reduction in luciferase activity when assessed individually. Notably, this suppressive effect is enhanced fourfold in cells expressing LAT transcript. Furthermore, both miRNAs significantly downregulate Conclusion: The study highlights the potential of targeting EphrinA3 through HSV-1-derived miRNAs, particularly miR-H2 and miR-H3, as a promising therapeutic strategy. These findings suggest that modulating EphrinA3 expression could enhance treatment efficacy while minimizing off-target effects, paving the way for innovative approaches to combat GBM. Further research is warranted to explore the clinical implications of these insights in developing effective therapies for this aggressive cancer.

Indexed as

EFNA3GBMHSV-1LAT-Derived miR-H2 and miR-H3

Identifiers

PMID40688500
PMCPMC12272618

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