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Am J Physiol Cell Physiol 278: C66-C72, 2000;
0363-6143/00 $5.00
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Vol. 278, Issue 1, C66-C72, January 2000

Tyrosine kinase inhibitors reduce bcl-2 expression and induce apoptosis in androgen-dependent cells

Takashi Ohigashi1,2, Munehisa Ueno1, Shoichi Nonaka1, Takashi Nakanoma1, Yusuke Furukawa3, Nobuhiro Deguchi1, and Masaru Murai2

1 Department of Urology, Kidney Center, Saitama Medical School, Moroyamamachi 350-0495; 3 Division of Hemopoiesis, Institute of Hematology and Department of Hematology, Jichi Medical School, Minamikawachimachi 329-0498; and 2 Department of Urology, School of Medicine, Keio University, Tokyo 160-8582, Japan

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.

protooncogene; mouse


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