Effects of arsenic trioxide on the cellular proliferation, apoptosis and differentiation of human neuroblastoma cells
Autor: | William M.W. Cheung, Yok L. Kwong, P Chu |
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Rok vydání: | 2007 |
Předmět: |
Cancer Research
Indoles Tyrosine 3-Monooxygenase Blotting Western Down-Regulation Apoptosis Caspase 3 Biology Tropomyosin receptor kinase A Arsenicals Neuroblastoma chemistry.chemical_compound Arsenic Trioxide Neurofilament Proteins Cell Line Tumor medicine Humans Receptor trkB Receptor trkA Arsenic trioxide Protein Kinase C Protein kinase C Cell Proliferation Neurons Dose-Response Relationship Drug Tyrosine hydroxylase Cell Differentiation Oxides medicine.disease Growth Inhibitors Up-Regulation Cell biology Enzyme Activation Oncology chemistry Trk receptor |
Zdroj: | Cancer Letters. 246:122-128 |
ISSN: | 0304-3835 |
DOI: | 10.1016/j.canlet.2006.02.009 |
Popis: | A human neuroblastoma cell line, IMR-32, was used as an in vitro model system to study the effects of arsenic trioxide (As(2)O(3)) on aggressive human neuroblastoma. From 0.5 micro M, As(2)O(3) exhibited a dose-dependent inhibition of IMR-32 proliferation. At concentrations of 1.5 micro M or higher, As(2)O(3) up-regulated caspase 3, leading to cellular apoptosis. However, neurofilament-200 kDa and tyrosine hydroxylase were not up-regulated, implying minimal neuronal differentiation. Concomitantly, TrkA was down-regulated and TrkB up-regulated. Pre-treatment with the protein kinase C (PKC) inhibitor Ro-31-8220 partially blocked As(2)O(3)-mediated apoptosis, meaning that As(2)O(3) might signal through PKC activation. The results suggest that As(2)O(3) might be potentially useful in neuroblastoma. |
Databáze: | OpenAIRE |
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