ArticleMolecular therapy. Nucleic acids2018
Cryptotanshinone Protects Cartilage against Developing Osteoarthritis through the miR-106a-5p/GLIS3 Axis.
Article in Molecular therapy. Nucleic acids, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 63 citations in OpenAlex.
- Methylation Landscapes of Cartilage in Hip Osteoarthritis.Genetics research · 2026Article
- Dual ferroptosis induction in N2-TANs and TNBC cells via FTH1 targeting: A therapeutic strategy for triple-negative breast cancer.Cell reports. Medicine · 2025Article
- Nutritional Epigenomics: Bioactive Dietary Compounds in the Epigenetic Regulation of Osteoarthritis.Pharmaceuticals (Basel, Switzerland) · 2024Review
- M2 macrophage-derived exosomal miR-26b-5p regulates macrophage polarization and chondrocyte hypertrophy by targeting TLR3 and COL10A1 to alleviate osteoarthritis.Journal of nanobiotechnology · 2024Article
- Pharmacological Mechanisms of Cryptotanshinone: Recent Advances in Cardiovascular, Cancer, and Neurological Disease Applications.Drug design, development and therapy · 2024Review
- Age-dependent genetic regulation of osteoarthritis: independent effects of immune system genes.Arthritis research & therapy · 2023Article
- Article
- Osteoarthritis related epigenetic variations in miRNA expression and DNA methylation.BMC medical genomics · 2023Article
- Disease-modifying therapeutic strategies in osteoarthritis: current status and future directions.Experimental & molecular medicine · 2021Review
- Article
- Cryptotanshinone interferes with chondrocyte apoptosis in osteoarthritis by inhibiting the expression of miR‑574‑5p.Molecular medicine reports · 2021Article
- Nuclear Magnetic Resonance Therapy Modulates the miRNA Profile in Human Primary OA Chondrocytes and Antagonizes Inflammation in Tc28/2a Cells.International journal of molecular sciences · 2021Article
- Combination of baicalein and miR-106a-5p mimics significantly alleviates IL-1β-induced inflammatory injury in CHON-001 cells.Experimental and therapeutic medicine · 2021Article
- Recent Advances in Pharmacological Intervention of Osteoarthritis: A Biological Aspect.Frontiers in pharmacology · 2021Review
- Role of MicroRNA, LncRNA, and Exosomes in the Progression of Osteoarthritis: A Review of Recent Literature.Orthopaedic surgery · 2020Review
- miR-140 Attenuates the Progression of Early-Stage Osteoarthritis by Retarding Chondrocyte Senescence.Molecular therapy. Nucleic acids · 2020Article
- miR-106a-5p Functions as a Tumor Suppressor by Targeting VEGFA in Renal Cell Carcinoma.Disease markers · 2020Article
- Long non-coding RNA H19 modulates proliferation and apoptosis in osteoarthritis via regulating miR-106a-5p.Journal of biosciences · 2019Article
- Dual regulatory roles of HMGB1 in inflammatory reaction of chondrocyte cells and mice.Cell cycle (Georgetown, Tex.) · 2019Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cryptotanshinone (CTS) has emerged as an anti-inflammatory agent in osteoarthritis (OA). However, the molecular mechanism underlying its potent therapeutic effect on OA remains largely unknown. MicroRNAs (miRNAs) act as crucial regulators in maintaining cartilage homeostasis. To investigate whether CTS protects against developing OA through regulation of miRNAs, we examined the potential CTS-mediated miRNA molecules using microarray analysis. We found that CTS significantly promoted miR-106a-5p expression in chondrocytes. Using the OA mouse model created by anterior cruciate ligament transection, we revealed that intra-articular injection of miR-106a-5p agomir attenuated OA. In addition, miR-106a-5p inhibited GLI-similar 3 (GLIS3) production by directly targeting the 3' untranslated region. CTS promoted miR-106a-5p expression through recruitment of a member of the paired box (PAX) family of transcription factors, PAX5, to the miR-106a-5p promoter. Inhibition of PAX5 mimicked the effect of miR-106a-5p and abolished the CTS ability to regulate miR-106a-5p expression. In OA patients, miR-106-5p is downregulated which is accompanied by downregulation of PAX5 and upregulation of GLIS3. Collectively, these data highlight that the PAX5/miR-106a-5p/GLIS3 axis acts as a novel pleiotropic regulator in CTS-mediated OA cartilage protection, suggesting that miR-106a-5p and PAX5 activation and GLIS3 inhibition might be useful and attractive for therapeutic strategies to treat OA patients.
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