ArticleAnnals of hematology2025
MiR-503-5p as a potential biomarker for deep venous thrombosis (DVT) in multiple myeloma (MM) and its role in disease development.
Article in Annals of hematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- The Role of Circulating MicroRNAs as Biomarkers and Therapeutic Targets in Venous Thromboembolism: A Systematic Review.Journal of clinical medicine · 2026Review
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9 authors.
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Abstract
Given the adverse impact of deep vein thrombosis (DVT) on the prognosis of multiple myeloma (MM) patients, identifying biomarkers for DVT is crucial for improving MM patient clinical outcomes. Therefore, this study aimed to evaluate the predictive value of miR-503-5p for DVT in MM, and explored the underlying mechanisms. Serum samples were collected from MM patients with and without DVT to measure miR-503-5p expression levels. ROC and Kaplan-Meier curves were employed to examine the predictive potential of miR-503-5p in MM-related DVT. MM serum-cultured human umbilical vein endothelial cells (HUVECs) were used to investigate the mechanisms of miR-503-5p in influencing the disease. Cell viability, oxidative stress status, and IL-6, TNF-α, TF, and TM levels were evaluated by CCK-8, antioxidant activity assay, and qRT-PCR. MiR-503-5p was upregulated in MM patients with DVT. The upregulation of miR-503-5p was a risk factor that demonstrated a high predictive value for DVT in MM patients. MiR-503-5p upregulation mediated the promotive effect of MM serum on HUVEC viability reduction, IL-6, TNF-α, and TF expression, and oxidative stress, and the inhibitory effect of MM serum on HUVEC TM expression. Moreover, WNT3A was a potential target of miR-503-5p in MM-related DVT. WNT3A downregulation mediated the effect of miR-503-5p on HUVECs. MiR-503-5p might be a promising biomarker for predicting DVT development in MM patients. MiR-503-5p might promote thrombosis in MM by affecting vein endothelial cells (VECs) through targeting WNT3A.
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