ArticleMolecular oncology2018
Role of TGF-β1/miR-382-5p/SOD2 axis in the induction of oxidative stress in CD34+ cells from primary myelofibrosis.
Article in Molecular oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- TGF-β/JNK axis mediates mitochondrial damage and macrophage cGAS-STING activation in liver Mallory-Denk body pathogenesis.Journal of translational medicine · 2025Article
- In Silico Prediction of Functional SNPs Interrupting Antioxidant Defense Genes in Relation to COVID-19 Progression.Biochemical genetics · 2025Article
- Chronic Inflammation in Primary Myelofibrosis: In-Depth Insights Into Pathogenesis and Promising Anti-Inflammatory Therapeutic Strategies.Mediators of inflammation · 2025Review
- Deepening Our Understanding of the Factors Affecting Landscape of Myeloproliferative Neoplasms: What Do We Know about Them?Cancers · 2023Review
- Mesenchymal stromal cells in tumor microenvironment remodeling of BCR-ABL negative myeloproliferative diseases.Frontiers in oncology · 2023Review
- Insights into Manganese Superoxide Dismutase and Human Diseases.International journal of molecular sciences · 2022Review
- Integrated bioinformatic analysis of dysregulated microRNA-mRNA co-expression network in ovarian endometriosis.Acta obstetricia et gynecologica Scandinavica · 2022Article
- Article
- Mechanism of microRNA regulating the progress of atherosclerosis in apoE-deficient mice.Bioengineered · 2021Article
- miR-495 Regulates Cellular Reactive Oxygen Species Levels by TargetingInfection and immunity · 2021Article
- Micro RNAs in Regulation of Cellular Redox Homeostasis.International journal of molecular sciences · 2021Review
- Inflammatory Microenvironment and Specific T Cells in Myeloproliferative Neoplasms: Immunopathogenesis and Novel Immunotherapies.International journal of molecular sciences · 2021Review
- Synergic Crosstalk between Inflammation, Oxidative Stress, and Genomic Alterations in BCR-ABL-Negative Myeloproliferative Neoplasm.Antioxidants (Basel, Switzerland) · 2020Review
- Revisiting cancer hallmarks: insights from the interplay between oxidative stress and non-coding RNAs.Molecular biomedicine · 2020Review
- circRNA-UBAP2 promotes the proliferation and inhibits apoptosis of ovarian cancer though miR-382-5p/PRPF8 axis.Journal of ovarian research · 2020Article
- Beyond JAK-STAT: novel therapeutic targets in Ph-negative MPN.Hematology. American Society of Hematology. Education Program · 2019Review
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by an excessive production of pro-inflammatory cytokines resulting in chronic inflammation and genomic instability. Besides the driver mutations in JAK2, MPL, and CALR genes, the deregulation of miRNA expression may also contribute to the pathogenesis of PMF. To this end, we recently reported the upregulation of miR-382-5p in PMF CD34+ cells. In order to unveil the mechanistic details of the role of miR-382-5p in pathogenesis of PMF, we performed gene expression profiling of CD34+ cells overexpressing miR-382-5p. Among the downregulated genes, we identified superoxide dismutase 2 (SOD2), which is a predicted target of miR-382-5p. Subsequently, we confirmed miR-382-5p/SOD2 interaction by luciferase assay and we showed that miR-382-5p overexpression in CD34+ cells causes the decrease in SOD2 activity leading to reactive oxygen species (ROS) accumulation and oxidative DNA damage. In addition, our data indicate that inhibition of miR-382-5p in PMF CD34+ cells restores SOD2 function, induces ROS disposal, and reduces DNA oxidation. Since the pro-inflammatory cytokine transforming growth factor-β1 (TGF-β1) is a key player in PMF pathogenesis, we further investigated the effect of TGF-β1 on ROS and miR-382-5p levels. Our data showed that TGF-β1 treatment enhances miR-382-5p expression and reduces SOD2 activity leading to ROS accumulation. Finally, inhibition of TGF-β1 signaling in PMF CD34+ cells by galunisertib significantly reduced miR-382-5p expression and ROS accumulation and restored SOD2 activity. As a whole, this study reports that TGF-β1/miR-382-5p/SOD2 axis deregulation in PMF cells is linked to ROS overproduction that may contribute to enhanced oxidative stress and inflammation. Our results suggest that galunisertib may represent an effective drug reducing abnormal oxidative stress induced by TGF-β1 in PMF patients. DATABASE LINKING: GEO: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE103464.
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