| Tyrosine kinase inhibitors reduce bcl-2 expression and induce apoptosis in androgen-dependent cells. | |
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MedLine Citation:
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PMID: 10644513 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The signal transduction pathway showing how androgen withdrawal induces apoptosis in androgen-dependent cells has not been clearly understood. In these studies, we focused on the behavior of tyrosine kinases in androgen-dependent cells and investigated its correlation with apoptosis and bcl-2 expression. We used SC2G, an androgen-dependent mouse mammary carcinoma cell line, which had been cloned from Shionogi Carcinoma 115 (SC115). When SC2G cells were cultured with herbimycin A (HMA), a potent tyrosine kinase inhibitor, the number of viable cells decreased significantly after 24 h. Terminal deoxyribonucleotidyltransferase-mediated dUTP-biotin nick end labeling and flow cytometric analysis of annexin V staining showed that HMA induced apoptosis of SC2G cells. The level of bcl-2 mRNA in SC2G cells was suppressed by HMA in a dose-dependent manner on RT-PCR. Preincubation with caspase inhibitors protected HMA-induced apoptosis of SC2G cells. When a human bcl-2 gene was transfected in SC2G cells and overexpressed, SC2G cells seemed to acquire tolerance for HMA. These data indicate that HMA-sensitive tyrosine kinase(s) can regulate apoptosis and inhibit bcl-2 expression in SC2G mouse androgen-dependent cells. Tyrosine kinase(s) seemed to be a member of signal transduction between androgen receptor activation and bcl-2 expression. |
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Authors:
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T Ohigashi; M Ueno; S Nonaka; T Nakanoma; Y Furukawa; N Deguchi; M Murai |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: American journal of physiology. Cell physiology Volume: 278 ISSN: 0363-6143 ISO Abbreviation: Am. J. Physiol., Cell Physiol. Publication Date: 2000 Jan |
Date Detail:
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Created Date: 2000-06-01 Completed Date: 2000-06-01 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 100901225 Medline TA: Am J Physiol Cell Physiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: C66-72 Citation Subset: IM |
Affiliation:
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Department of Urology, Kidney Center, Saitama Medical School, Moroyamamachi 350-0495, Japan. ohigashi@med.keio.ac.jp |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / drug effects, physiology* Benzoquinones Caspases / metabolism Cell Separation Cell Survival / drug effects, physiology Cysteine Proteinase Inhibitors / pharmacology Dose-Response Relationship, Drug Enzyme Inhibitors / pharmacology Gene Expression Regulation, Enzymologic / drug effects Gonadal Steroid Hormones / pharmacology* Humans In Situ Nick-End Labeling Lactams, Macrocyclic Mammary Neoplasms, Experimental Mice Oligopeptides / pharmacology Protein-Tyrosine Kinases / antagonists & inhibitors*, metabolism Proto-Oncogene Proteins c-bcl-2 / genetics* Quinones / pharmacology RNA, Messenger / analysis Testosterone / pharmacology* Transfection Tumor Cells, Cultured / cytology, drug effects, enzymology |
| Chemical | |
Reg. No./Substance:
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0/Benzoquinones; 0/Cysteine Proteinase Inhibitors; 0/Enzyme Inhibitors; 0/Gonadal Steroid Hormones; 0/Lactams, Macrocyclic; 0/Oligopeptides; 0/Proto-Oncogene Proteins c-bcl-2; 0/Quinones; 0/RNA, Messenger; 0/acetyl-aspartyl-glutamyl-valyl-aspartal; 143313-51-3/L 709049; 58-22-0/Testosterone; 70563-58-5/herbimycin; EC 2.7.10.1/Protein-Tyrosine Kinases; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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