期刊
PHARMACOLOGY
卷 94, 期 3-4, 页码 163-169出版社
KARGER
DOI: 10.1159/000368050
关键词
Naftopidil; Malignant pleural mesothelioma; Apoptosis; Tumor necrosis factor-alpha; FasL; Cancer therapy
资金
- Takeda Science Foundation
- MEXT-Supported Program for the Strategic Research Foundation at Private Universities
Naftopidil, an alpha(1)-adrenoceptor blocker, induced apoptosis of human malignant pleural mesothelioma NCI-H2052 cells. Naftopidil upregulated the expression of tumor necrosis factor-alpha (TNF-alpha) 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-alpha 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. (C) 2014 S. Karger AG, Basel
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