ArticleThe Korean journal of pain2025
MiR-298 suppresses astrocytic NF-κB activity and neuroinflammation
Article in The Korean journal of pain, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Subtype-Independent Activation of NF-κB Signaling in Breast Cancer.International journal of molecular sciences · 2026Article
- Downregulation of lncRNA HOTTIP alleviates neuropathic pain and inflammation in chronic constriction injury rats by targeting miR-216a-5p.The Korean journal of pain · 2026Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Bone cancer pain (BCP), a major symptom impairing quality of life and mobility in cancer patients, is linked to microRNAs dysregulation. This study investigates the role of miR-298 in a mouse BCP model established by implanting tumor cells into the femoral marrow cavity. Methods: Forty-eight male C3H/HeJ mice were randomized into sham or tumor groups, receiving intrathecal miR- 298 agonist/antagonist or controls. Behavioral assessments (paw withdrawal mechanical threshold [PWMT] and number of spontaneous flinches [NSF]) were performed before and after surgery (days 0, 4, 7, 10, 14, 21, 28). Astrocyte activation, inflammatory cytokines, and pathway proteins (MyD88, TAK1, p-p65) were analyzed via quantitative Reverse Transcription Polymerase Chain Reaction (qRT-PCR), Western blot, and immunofluorescence. Statistical analysis used one-way ANOVA with Tukey's test and independent t-tests ( Results: Tumor-implanted mice showed significant mechanical hypersensitivity in PWMT and NSF versus sham controls ( Conclusions: MiR-298 reduces BCP in mice by inhibiting astrocyte-mediated neuroinflammation and blocking the MyD88/NF-κB pathway.
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