ArticleCell cycle (Georgetown, Tex.)2013
miR-29b induces SOCS-1 expression by promoter demethylation and negatively regulates migration of multiple myeloma and endothelial cells.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 96 citations in OpenAlex.
- Deciphering epigenetic crosstalk in multiple myeloma pathogenesis and treatment.Clinical epigenetics · 2026Review
- MicroRNA in cancer therapy: breakthroughs and challenges in early clinical applications.Journal of experimental & clinical cancer research : CR · 2025Review
- The multi-faceted roles of cancer-associated fibroblasts in pancreatic cancer.Cellular signalling · 2025Review
- Multiple Myeloma: Genetic and Epigenetic Biomarkers with Clinical Potential.International journal of molecular sciences · 2024Article
- Review
- Lipid metabolic vulnerabilities of multiple myeloma.Clinical and experimental medicine · 2023Review
- Cancer-associated fibroblast-derived exosome microRNA-21 promotes angiogenesis in multiple myeloma.Scientific reports · 2023Article
- Natural Agents as Novel Potential Source of Proteasome Inhibitors with Anti-Tumor Activity: Focus on Multiple Myeloma.Molecules (Basel, Switzerland) · 2023Review
- MiRNA as a Potential Target for Multiple Myeloma Therapy-Current Knowledge and Perspectives.Journal of personalized medicine · 2022Review
- Mitochondrial Determinants of Anti-Cancer Drug-Induced Cardiotoxicity.Biomedicines · 2022Review
- miRNAs as Biomarkers and Possible Therapeutic Strategies in Synovial Sarcoma.Frontiers in pharmacology · 2022Review
- MicroRNAs as a Potential New Preventive Approach in the Transition from Asymptomatic to Symptomatic Multiple Myeloma Disease.Cancers · 2021Review
- Adulthood blood levels of hsa-miR-29b-3p associate with preterm birth and adult metabolic and cognitive health.Scientific reports · 2021Article
- Crosstalk Between Inflammatory Signaling and Methylation in Cancer.Frontiers in cell and developmental biology · 2021Review
- Role of microRNAs in Diagnosis, Prognosis and Management of Multiple Myeloma.International journal of molecular sciences · 2020Review
- Non-Coding RNAs in Multiple Myeloma Bone Disease Pathophysiology.Non-coding RNA · 2020Review
- Non-coding RNAs in cancer: platforms and strategies for investigating the genomic "dark matter".Journal of experimental & clinical cancer research : CR · 2020Review
- The Non-Coding RNA Landscape of Plasma Cell Dyscrasias.Cancers · 2020Review
- MicroRNAs Associated With a Good Prognosis of Acute Myeloid Leukemia and Their Effect on Macrophage Polarization.Frontiers in immunology · 2020Review
- A Comprehensive Biological and Clinical Perspective Can Drive a Patient-Tailored Approach to Multiple Myeloma: Bridging the Gaps between the Plasma Cell and the Neoplastic Niche.Journal of oncology · 2020Review
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Authors and funding
16 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epigenetic silencing of tumor suppressor genes frequently occurs and may account for their inactivation in cancer cells. We previously demonstrated that miR-29b is a tumor suppressor microRNA (miRNA) that targets de novo DNA methyltransferases and reduces the global DNA methylation of multiple myeloma (MM) cells. Here, we provide evidence that epigenetic activity of miR-29b leads to promoter demethylation of suppressor of cytokine signaling-1 (SOCS-1), a hypermethylated tumor suppressor gene. Enforced expression of synthetic miR-29b mimics in MM cell lines resulted in SOCS-1 gene promoter demethylation, as assessed by Sequenom MassARRAY EpiTYPER analysis, and SOCS-1 protein upregulation. miR-29b-induced SOCS-1 demethylation was associated with reduced STAT3 phosphorylation and impaired NFκB activity. Downregulation of VEGF-A and IL-8 mRNAs could be detected in MM cells transfected with miR-29b mimics as well as in endothelial (HUVEC) or stromal (HS-5) cells treated with conditioned medium from miR-29b-transfected MM cells. Notably, enforced expression of miR-29b mimics increased adhesion of MM cells to HS-5 and reduced migration of both MM and HUVEC cells. These findings suggest that miR-29b is a negative regulator of either MM or endothelial cell migration. Finally, the proteasome inhibitor bortezomib, which induces the expression of miR-29b, decreased global DNA methylation by a miR-29b-dependent mechanism and induced SOCS-1 promoter demethylation and protein upregulation. In conclusion, our data indicate that miR-29b is endowed with epigenetic activity and mediates previously unknown functions of bortezomib in MM cells.
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