ArticleMolecular neurobiology2022
LncRNA SNHG25 Promotes Glioma Progression Through Activating MAPK Signaling.
Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Associating cancer-related RNA structure disrupting SNPs in LincRNAs to function.BMC genomics · 2025Article
- LncRNA PSMA-AS1 affects glioma cell metastasis through mediating pyroptosis via miR-140-3p/SRSF10 axis.Cytotechnology · 2025Article
- Annexin A2: regulating glioma's fate and a potential therapeutic target.Medical oncology (Northwood, London, England) · 2025Article
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- Calnexin promotes glioblastoma progression by inducing protective mitophagy through the MEK/ERK/BNIP3 pathway.Theranostics · 2025Article
- Bioinformatics Analysis Reveals the Oncogenic Role and Therapeutic Potential of lncRNA SNHG25 in Colon Adenocarcinoma.International journal of genomics · 2025Article
- Identification of candidate plasma miRNA biomarkers for the diagnosis of head and neck squamous cell carcinoma.Future science OA · 2024Article
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Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Numerous studies indicated that long non-coding RNAs (lncRNAs) play critical roles in glioma initiation and progression. SNHG25 is a newly identified lncRNA. And the functional role and molecular mechanism of SNHG25 in glioma cells have not been investigated. In this study, we found that SNHG25 was upregulated in glioma cells and tissues. CCK-8, EDU, and colony formation assays demonstrated that SNHG25 knockdown markedly inhibited glioma cell proliferation. In vivo studies showed that SNHG25 knockdown significantly inhibited tumor growth. Further studies indicated that SNHG25 positively regulated MAP2K2 through sponging miR-579-5p. High expression of SNHG25 activated MAPK signaling through MAP2K2. These data suggest that SNHG25 is a potential target and biomarker for glioma.
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Registered trials
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