Abstract
In view of a potential clinical use, we assessed the antiproliferative effect of paclitaxel on the human steroid-secreting NCI-H295 adrenocarcinoma cell line. By MTT, paclitaxel induced a dose-dependent inhibition of cell proliferation, with IC50 lower than blood levels of the drug achieved in patients treated for other malignancies. Cell exposure to paclitaxel for 24 h at the different IC50S produced a dose-responsive increase in DNA fragmentation, morphologically confirmed by electron microscopy. A time-dependent decrease in aldosterone, cortisol and testosterone was observed. Paclitaxel is an effective antiproliferative agent in this human adrenocortical carcinoma cell line. Apoptosis induced by the drug in involved in neoplastic cell death. A potential role of the drug in the treatment of patients with adrenocortical cancer could be considered.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adrenal Cortex Neoplasms / drug therapy*
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Adrenal Cortex Neoplasms / ultrastructure
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Adrenocortical Carcinoma / drug therapy*
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Adrenocortical Carcinoma / ultrastructure
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Aldosterone / metabolism
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Antineoplastic Agents, Phytogenic / administration & dosage
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Antineoplastic Agents, Phytogenic / pharmacology*
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Apoptosis / drug effects
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Cell Division / drug effects
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Chromatin / drug effects
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Chromatin / pathology
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Culture Media, Conditioned / chemistry
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Culture Media, Conditioned / metabolism
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Cytoplasm / drug effects
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Cytoplasm / pathology
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DNA Fragmentation / drug effects
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Dose-Response Relationship, Drug
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Humans
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Hydrocortisone / metabolism
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Microscopy, Electron
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Paclitaxel / administration & dosage
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Paclitaxel / pharmacology*
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Testosterone / metabolism
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Time Factors
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Tumor Cells, Cultured
Substances
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Antineoplastic Agents, Phytogenic
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Chromatin
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Culture Media, Conditioned
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Testosterone
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Aldosterone
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Paclitaxel
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Hydrocortisone