ArticleGenes & genomics2020
miR-300 mitigates cancer-induced bone pain through targeting HMGB1 in rat models.
Article in Genes & genomics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Chemotherapy-derived DAMPs drive reprogramming of tumor-associated macrophages toward a pro-inflammatory phenotype in hepatocellular carcinoma.Scientific reports · 2026Article
- The influence of neuro-tumor interactions on tumorigenesis and therapeutic response.Experimental hematology & oncology · 2026Review
- The Efficacy of Intrathecal Platelet-Rich Plasma Administration in Alleviation of Chronic Neuropathic Pain in Rat Model.Molecular neurobiology · 2025Article
- The role of non-coding RNAs in neuropathic pain.Pflugers Archiv : European journal of physiology · 2024Review
- Multiple functions of HMGB1 in cancer.Frontiers in oncology · 2024Review
- Hmgb1 Silencing in the Amygdala Inhibits Pain-Related Behaviors in a Rat Model of Neuropathic Pain.International journal of molecular sciences · 2023Article
- The impacts of exosomes on bone metastatic progression and their potential clinical utility.Bone reports · 2022Article
- Knockdown of PAR2 alleviates cancer-induced bone pain by inhibiting the activation of astrocytes and the ERK pathway.BMC musculoskeletal disorders · 2022Article
- The emerging power and promise of non-coding RNAs in chronic pain.Frontiers in molecular neuroscience · 2022Review
- microRNA-Based Network and Pathway Analysis for Neuropathic Pain in Rodent Models.Frontiers in molecular biosciences · 2021Article
- Antinociceptive effects of macrophage-derived extracellular vesicles by carrying microRNA-216a.American journal of translational research · 2021Article
- Platelet-rich plasma improves chronic inflammatory pain by inhibiting PKM2-mediated aerobic glycolysis in astrocytes.Annals of translational medicine · 2020Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCancer-induced bone pain (CIBP) is the pain caused by bone metastasis from malignant tumors, and the largest source of pain for cancer patients. miR-300 is an important miRNA in cancer. It has been shown that miR-300 regulates tumorigenesis of various tumors.
objectiveThis study aims to investigate the role of miR-300 in CIBP and its underlying molecular mechanisms in vitro and in vivo.
methodsWe constructed CIBP model in rats and investigated the mechanism through which miR-300 affects CIBP. We first examined expression level of miR-300 in CIBP rats and then tested the effect of its overexpression. Next, we identified the target of miR-300 using TargetScan analysis and double luciferase assay. Finally, we studied genetic interactions between miR-300 and its target and their roles in CIBP.
resultsWe found that miR-300 was downregulated in CIBP rats. Overexpression of miR-300 significantly attenuated cancer-induced neuropathic pain (p < 0.01). Furthermore, TargetScan analysis and double luciferase assay show High Mobility Group Box 1 (HMGB1) is a target of miR-300. Notably, HMGB1 is overexpressed in CIBP rats, while up-regulation of miR-300 significantly suppresses expression of HMGB1 (p < 0.01). Moreover, knockdown of HMGB1 by siRNA significantly relieves cancer-induced neuropathic pain in rats (p < 0.01). On the other hand, HMGB1 overexpression partially blocked the effect of miR-300 on cancer-induced nerve pain.
conclusionmiR-300 relieves cancer-induced neuropathic pain by inhibiting HMGB1 expression. These results may be beneficial for the treatment of CIBP in clinical practice.
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