ArticleInternational journal of molecular sciences2018
MLN4924, a Protein Neddylation Inhibitor, Suppresses the Growth of Human Chondrosarcoma through Inhibiting Cell Proliferation and Inducing Endoplasmic Reticulum Stress-Related Apoptosis.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
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- The cGAS-STING Pathway: A Double-Edged Regulator of Neuroinflammation and Myelin Regeneration.Molecular neurobiology · 2026Review
- Evaluation of the safety and efficacy of pressure-enhanced scar patch in a rabbit ear hypertrophic scar model.Journal of molecular histology · 2026Article
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- Nell-1 inhibits osteoclast differentiation and bone resorption in apical periodontitis.Journal of molecular histology · 2026Article
- Effect of somatosensory games on arterial stiffness and antioxidant status in postmenopausal women.European journal of applied physiology · 2026Article
- C-Jun NH2-terminal kinase inhibitor bentamapimod prevents RANKL-mediated osteoclastogenesis and ovariectomy-induced osteoporosis.In vitro cellular & developmental biology. Animal · 2026Article
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- Molecular mechanisms in endometriosis: linking JAK/STAT pathway, ferroptosis, and microbial dysbiosis.Molecular biology reports · 2026Review
- Research Trends and Hotspots in Hypertrophic Scar: A Bibliometric Analysis over the Past Five Decades.Aesthetic plastic surgery · 2025Article
- Targeting pregnane X receptor with a potent agonist-based PROTAC to delay colon cancer relapse.Oncogenesis · 2025Article
- MeWRKY30, a cassava stress-responsive WRKY transcription factor, confers drought resistance to transgenic Arabidopsis.Plant cell reports · 2025Article
- Comprehensive analysis Neddylation-related genes identified UBB as a prognostic biomarker for clear cell renal cell carcinoma.Discover oncology · 2025Article
- Article
- Proteasomal deubiquitinating enzyme USP14/UCHL5 inhibitor bAP15 suppresses endoplasmic reticulum stress-mediated apoptosis and tumor growth in human chondrosarcoma.American journal of cancer research · 2025Article
- High-Throughput Drug Screening in Chondrosarcoma Cells Identifies Effective Antineoplastic Agents Independent of IDH Mutation.International journal of molecular sciences · 2024Article
- Genetics and Molecular Pathogenesis of the Chondrosarcoma: A Review of the Literature.Current issues in molecular biology · 2024Review
- Drugs targeting TGF-β/Notch interaction attenuate hypertrophic scar formation by optic atrophy 1-mediated mitochondrial fusion.Molecular and cellular biochemistry · 2024Article
- RNF2 promotes chondrosarcoma progression by regulating ubiquitination and degradation of CBX7.Cancer & metabolism · 2024Article
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
Chondrosarcoma, a heterogeneous malignant bone tumor, commonly produces cartilage matrix, which generally has no response to conventional therapies. Studies have reported that MLN4924, a NEDD8-activating enzyme inhibitor, achieves antitumor effects against numerous malignancies. In this study, the suppressive effects of MLN4924 on human chondrosarcoma cell lines were investigated using in vitro and in vivo assays, which involved measuring cell viability, cytotoxicity, apoptosis, proliferation, cell cycles, molecule-associated cell cycles, apoptosis, endoplasmic reticulum (ER) stress, and tumor growth in a xenograft mouse model. Our results demonstrated that MLN4924 significantly suppressed cell viability, exhibited cytotoxicity, and stimulated apoptosis through the activation of caspase-3 and caspase-7 in chondrosarcoma cell lines. Furthermore, MLN4924 significantly inhibited cell proliferation by diminishing the phosphorylation of histone H3 to cause G2/M cell cycle arrest. In addition, MLN4924 activated ER stress⁻related apoptosis by upregulating the phosphorylation of c-Jun N-terminal kinase (JNK), enhancing the expression of GRP78 and CCAAT-enhancer-binding protein homologous protein (CHOP, an inducer of endoplasmic ER stress⁻related apoptosis) and activating the cleavage of caspase-4. Moreover, MLN4924 considerably inhibited the growth of chondrosarcoma tumors in a xenograft mouse model. Finally, MLN4924-mediated antichondrosarcoma properties can be accompanied by the stimulation of ER stress⁻related apoptosis, implying that targeting neddylation by MLN4924 is a novel therapeutic strategy for treating chondrosarcoma.
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Registered trials
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