Cell cycle arrest and apoptosis induced by kinamycin f in human osteosarcoma cells

التفاصيل البيبلوغرافية
العنوان: Cell cycle arrest and apoptosis induced by kinamycin f in human osteosarcoma cells
المؤلفون: Enrico Focaccia, Irene Faenza, Alberto Bavelloni, Manuela Piazzi, Costantino Errani, William L. Blalock
المساهمون: Bavelloni, Alberto, Focaccia, Enrico, Piazzi, Manuela, Errani, Costantino, Blalock, William, Faenza, Irene
سنة النشر: 2017
مصطلحات موضوعية: 0301 basic medicine, Cell death, G2 Phase, Cancer Research, Cell cycle checkpoint, Cell Survival, Cyclin A, Cell, Population, Antineoplastic Agents, Apoptosis, Antineoplastic Agent, 03 medical and health sciences, Cell Cycle Checkpoint, Cell Line, Tumor, medicine, Humans, Viability assay, Cyclin D3, education, Cell Proliferation, education.field_of_study, Osteosarcoma, biology, Cell growth, Chemistry, Quinones, Apoptosi, General Medicine, Cell Cycle Checkpoints, Molecular biology, 030104 developmental biology, medicine.anatomical_structure, Oncology, biology.protein, Quinone, Kinamycin F, Human
الوصف: Background/aim Kinamycin F is a bacterial metabolite which contains an unusual and potentially reactive diazo group that is known for its ability to inhibit cell growth. In this study, the potential anti-tumor activity of kinamycin F was investigated in three human osteosarcoma cell lines, MG-63, U-2 OS and HOS as an antitumor agent with a potentially novel target. Materials and methods Proliferation and cell viability were measured in three human osteosarcoma cell lines by commercially available kits. We also evaluated the effects of the drug on cell cycle progression using the Muse™ Cell Analyzer. Caspase-3 activity was determined by a fluorometric EnzChek assay kit. Finally, following treatment with kinamycin F the protein levels of cyclin D3, cyclin A and cdK-2 were examined. Results Kinamycin F induced a concentration-dependent cell death in all the three cell lines. Flow cytometry revealed that kinamycin F treatment at 1 μM concentration significantly increased the cell population in the G2/M-phase (60-65%). Kinamycin F activated caspase 3 in all the three cell lines, clearly demonstrating that the growth inhibitory effect of kinamycin F can be attributed to apoptosis induction. Finally, kinamycin F suppressed osteosarcoma cell proliferation affecting cyclin A and D3 expression. Conclusion Understanding the mechanism by which kinamycin F exerts its ability to inhibit cell growth may be a step forward in the development of new therapeutic strategies for the treatment of OS.
وصف الملف: STAMPA
اللغة: English
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2fb6bb601eda73227ef5f3a43f30f403Test
http://hdl.handle.net/11585/609384Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....2fb6bb601eda73227ef5f3a43f30f403
قاعدة البيانات: OpenAIRE