Abstract
Naftopidil, an α1-adrenoceptor blocker, induced apoptosis of human malignant pleural mesothelioma NCI-H2052 cells. Naftopidil upregulated the expression of tumor necrosis factor-α (TNF-α) mRNA in these cells. Naftopidil, alternatively, increased FasL secretion from NCI-H2052 cells, without affecting the expression of FasL mRNA and protein, and activated caspase-3 and -8 in NCI-H2052 cells. Naftopidil drastically suppressed tumor growth in mice inoculated with these cells. The results of the present study indicate that naftopidil induces apoptosis of NCI-H2052 cells by upregulating the expression of TNF-α and stimulating the secretion of FasL, a ligand for the death receptor Fas, both to activate caspase-8 and the effector caspase-3, leading to the suppression of NCI-H2052 cell proliferation in vivo. This raises the possibility that naftopidil could be developed as an effective drug for the treatment of malignant pleural mesothelioma.
© 2014 S. Karger AG, Basel.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adrenergic alpha-Antagonists / pharmacology
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Adrenergic alpha-Antagonists / therapeutic use*
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Animals
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use*
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Apoptosis / drug effects
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Caspase 3 / metabolism
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Caspase 8 / metabolism
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Caspase 9 / metabolism
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Cell Line, Tumor
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Fas Ligand Protein / genetics
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Fas Ligand Protein / metabolism
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Humans
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Lung Neoplasms / drug therapy*
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Lung Neoplasms / pathology
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Male
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Mesothelioma / drug therapy*
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Mesothelioma / pathology
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Mesothelioma, Malignant
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Mice, Nude
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Naphthalenes / pharmacology
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Naphthalenes / therapeutic use*
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Piperazines / pharmacology
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Piperazines / therapeutic use*
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RNA, Messenger / metabolism
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Tumor Burden / drug effects
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Tumor Necrosis Factor-alpha / genetics
Substances
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Adrenergic alpha-Antagonists
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Antineoplastic Agents
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Fas Ligand Protein
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Naphthalenes
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Piperazines
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RNA, Messenger
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Tumor Necrosis Factor-alpha
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CASP8 protein, human
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Caspase 3
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Caspase 8
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Caspase 9
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naftopidil