cerivastatin has been researched along with Osteosarcoma* in 2 studies
2 other study(ies) available for cerivastatin and Osteosarcoma
| Article | Year |
|---|---|
Identification of potential modulators of osteosarcoma metastasis by high-throughput cellular screening of natural products.
A high-throughput screening assay was developed and applied to a large library of natural product extract samples, in order to identify compounds which preferentially inhibited the in vitro 2D growth of a highly metastatic osteosarcoma cell line (MG63.3) compared to a cognate parental cell line (MG63) with low metastatic potential. Evaluation of differentially active natural product extracts with bioassay-guided fractionation led to the identification of lovastatin (IC Topics: Biological Products; Bone Neoplasms; Cell Line; Cell Movement; Cell Proliferation; Cell Survival; Drugs, Chinese Herbal; High-Throughput Screening Assays; Humans; Lovastatin; Melia; Monascus; Osteosarcoma; Plant Extracts; Pyridines; Seeds | 2021 |
RhoA GTPase inactivation by statins induces osteosarcoma cell apoptosis by inhibiting p42/p44-MAPKs-Bcl-2 signaling independently of BMP-2 and cell differentiation.
Osteosarcoma is the most common primary bone tumour in young adults. Despite improved prognosis, resistance to chemotherapy remains responsible for failure of osteosarcoma treatment. The identification of signals that promote apoptosis may provide clues to develop new therapeutic strategies for chemoresistant osteosarcoma. Here, we show that lipophilic statins (atorvastatin, simvastatin, cerivastatin) markedly induce caspases-dependent apoptosis in various human osteosarcoma cells, independently of bone morphogenetic protein (BMP)-2 signaling and cell differentiation. Although statins increased BMP-2 expression, the proapoptotic effect of statins was not prevented by the BMP antagonist noggin, and was abolished by mevalonate and geranylgeranylpyrophosphate, suggesting the involvement of defective protein geranylgeranylation. Consistently, lipophilic statins induced membrane RhoA relocalization to the cytosol and inhibited RhoA activity, which resulted in decreased phospho-p42/p44- mitogen-activated protein kinases (MAPKs) and Bcl-2 levels. Constitutively active RhoA rescued phospho-p42/p44-MAPKs and Bcl-2 and abolished statin-induced apoptosis. Thus, lipophilic statins induce caspase-dependent osteosarcoma cell apoptosis by a RhoA-p42/p44 MAPKs-Bcl-2-mediated mechanism, independently of BMP-2 signaling and cell differentiation. Topics: Anticholesteremic Agents; Apoptosis; Atorvastatin; Bone Morphogenetic Protein 2; Bone Morphogenetic Proteins; Caspases; Cell Differentiation; Cell Survival; Enzyme Activation; Extracellular Signal-Regulated MAP Kinases; Gene Expression Regulation, Neoplastic; Heptanoic Acids; Humans; Osteosarcoma; Phenotype; Phosphorylation; Polyisoprenyl Phosphates; Protein Transport; Proto-Oncogene Proteins c-bcl-2; Pyridines; Pyrroles; rhoA GTP-Binding Protein; RNA, Messenger; Signal Transduction; Simvastatin; Transforming Growth Factor beta | 2006 |