Troglitazione affects survival of human osteosarcoma cells
Autor: | Giuliana Gobbi, Luca Sangiorgi, Sandra Marmiroli, Enrico Lucarelli, Giovanna Lattanzi, Marina Mordenti, Francesca Scrimieri, Annarosa Zambon Bertoja, Piero Picci, Veronica Maini, Matteo Reggiani |
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Jazyk: | angličtina |
Rok vydání: | 2002 |
Předmět: |
Cancer Research
medicine.medical_specialty Cell Survival Blotting Western Receptors Cytoplasmic and Nuclear Peroxisome proliferator-activated receptor Antineoplastic Agents Apoptosis Bone Neoplasms Cell Count Protein Serine-Threonine Kinases Biology troglitazone survival PPAR agonist Troglitazone Proto-Oncogene Proteins Internal medicine Tumor Cells Cultured medicine Humans Chromans Receptor Transcription factor Protein kinase B chemistry.chemical_classification Osteosarcoma Precipitin Tests Thiazoles Endocrinology Oncology chemistry Cell culture saos2 osteosarcoma cells Cancer research Thiazolidinediones Proto-Oncogene Proteins c-akt Cell Division Transcription Factors medicine.drug |
Popis: | Activation of PPAR gamma, a transcription factor member of the family of peroxisome proliferator-activated receptors, induces apoptosis in several normal and tumor cell lines. In our study, we investigated whether treatment with troglitazone (TRO), a known PPAR gamma agonist, induced apoptosis in the human osteosarcoma (OS) cell lines G292, MG63, SAOS and U2OS that express PPAR gamma. In our experiments, TRO never induced apoptosis of OS cells; on the contrary, TRO increased cell number, based on MTT proliferation assay. Remarkably, the TRO-induced cell number increase depended on a decrease of apoptosis that naturally occurred in the culture and was not due to an increased cell proliferation rate. TRO also prevented staurosporin-induced apoptosis. The TRO-mediated survival effect correlated with the activation of Akt, a well-known mediator of survival stimuli. Our work describes a new function for TRO and indicates that the Akt survival pathway may be a mediator of TRO-induced increase of survival. |
Databáze: | OpenAIRE |
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