ArticleDiagnostic pathology2019
LncRNA DNM3OS promotes proliferation and inhibits apoptosis through modulating IGF1 expression by sponging MiR-126 in CHON-001 cells.
Article in Diagnostic pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- Non-Coding RNAs in Gastrointestinal Stromal Tumors: Regulatory Networks, Drug Resistance, and Clinical Implications.International journal of molecular sciences · 2026Review
- Article
- Acupuncture alleviates the progression of knee osteoarthritis by inhibiting X-inactive specific transcript-mediated activation of the mechanosensitive ion channel Piezo1 signaling.Nagoya journal of medical science · 2025Article
- Long Non-coding RNA DNM3OS: Pathogenic Roles and Molecular Mechanisms in Pathophysiological Processes.Current medicinal chemistry · 2024Review
- DNM3OS Enhances the Apoptosis and Senescence of Spermatogonia Associated with Nonobstructive Azoospermia by Providing miR-214-5p and Decreasing E2F2 Expression.Analytical cellular pathology (Amsterdam) · 2023Article
- Engineering of MSC-Derived Exosomes: A Promising Cell-Free Therapy for Osteoarthritis.Membranes · 2022Review
- LncRNA MAFG-AS1 promotes the malignant phenotype of ovarian cancer by upregulating NFKB1-dependent IGF1.Cancer gene therapy · 2022Article
- Comparison of lncRNA Expression in the Uterus between Periods of Embryo Implantation and Labor in Mice.Animals : an open access journal from MDPI · 2022Article
- Emerging role of lncRNAs in osteoarthritis: An updated review.Frontiers in immunology · 2022Review
- Long non-coding RNA MCM3AP-AS1 protects chondrocytes ATDC5 and CHON-001 from IL-1β-induced inflammation via regulating miR-138-5p/SIRT1.Bioengineered · 2021Article
- Integrated analysis of long non-coding RNAs and mRNAs associated with malignant transformation of gastrointestinal stromal tumors.Cell death & disease · 2021Article
- Long non-coding RNA KCNQ1OT1 promotes cell viability and migration as well as inhibiting degradation of CHON-001 cells by regulating miR-126-5p/TRPS1 axis.Advances in rheumatology (London, England) · 2021Article
- Long non-coding RNA GAS5 suppresses rheumatoid arthritis progression via miR-128-3p/HDAC4 axis.Molecular and cellular biochemistry · 2021Article
- LncRNA DNM3OS regulates GREM2 via miR-127-5p to suppress early chondrogenic differentiation of rat mesenchymal stem cells under hypoxic conditions.Cellular & molecular biology letters · 2021Article
- Up-regulation of long non-coding RNA CYTOR induced by icariin promotes the viability and inhibits the apoptosis of chondrocytes.BMC complementary medicine and therapies · 2021Article
- A novel tumor suppressor ASMTL-AS1 regulates the miR-1228-3p/SOX17/β-catenin axis in triple-negative breast cancer.Diagnostic pathology · 2021Article
- The function of lncRNAs in the pathogenesis of osteoarthritis.Bone & joint research · 2021Article
- lncRNA SNHG16 promotes the occurrence of osteoarthritis by sponging miR‑373‑3p.Molecular medicine reports · 2021Article
- Recent Advances in Pharmacological Intervention of Osteoarthritis: A Biological Aspect.Frontiers in pharmacology · 2021Review
- Interactions Among lncRNA/circRNA, miRNA, and mRNA in Musculoskeletal Degenerative Diseases.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAs a degenerative disease, osteoarthritis (OA) greatly affects aged population. The human chondrocyte cell line CHON-001, derived from normal human articular cartilage, has been widely used in vitro in osteoarthritis models. In order to better understand the underlying mechanism of OA pathogenesis, this study was conducted to explore the effects of LncRNA dynamin 3 opposite strand (DNM3OS) on CHON-001 cells.
methodsThe expression levels of and correlation between DNM3OS and miR-126 that derived from OA and non-OA tissues were determined by quantitative real time (qRT)-PCR and Spearman's correlation analysis. Cell viability, clone, migration, invasion and apoptosis were respectively determined by cell counting kit-8, colony formation, wound healing assay, transwell and flow cytometry. The target genes were predicted by starbase V2 and targetscan 7.2 and confirmed by luciferase reporter assay. The expressions of apoptosis-related factors were detected by Western blot.
resultsThe expression of DNM3OS was down-regulated in OA patients. Functional assays demonstrated that ectopic expression of DNM3OS promoted the proliferation and inhibited apoptosis of CHON-001 cells, and that knocking down DNM3OS suppressed cell proliferation and induced apoptosis. Mechanistic investigation revealed that DNM3OS physically bound to the promoter of miR-126 and suppressed miR-126 expression. Decreased expression of DNM3OS was negatively correlated with miR-126 in OA patients. Furthermore, the effects of siDNM3OS on inhibiting cell proliferation and promoting apoptosis were partially reversed by miR-126 inhibitor. Meanwhile, type insulin-like growth factor-1 (IGF1) was identified as a target gene for miR-126 and was negatively associated with the miR-126 expression. Overexpressed IGF1 restored the effects of miR-126 mimic in suppressing cell proliferation and promoting apoptosis.
conclusionOur results showed that DNM3OS could affect the CHON-001 cell proliferation and apoptosis by regulating IGF1 by sponging miR-126.
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