Adenovirus-mediated high expression of BCL-6 in CV-1 cells induces apoptotic cell death accompanied by down-regulation of BCL-2 and BCL-XL

被引:0
作者
Tadanori Yamochi
Yoshitaka Kaneita
Tetsu Akiyama
Shigeo Mori
Masatsugu Moriyama
机构
[1] the Institute of Medical Science,Department of Pathology
[2] the University of Tokyo,Department of Oncogene Research
[3] 4-6-1,undefined
[4] Research Institute for Microbial Diseases,undefined
[5] Osaka University,undefined
来源
Oncogene | 1999年 / 18卷
关键词
BCL-6; apoptosis; cell cycle; BCL-2; recombinant adenovirus;
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中图分类号
学科分类号
摘要
The BCL-6 proto-oncogene encodes a 92- to 98-kDa transcriptional repressor containing the BTB/POZ domain at its N-terminal region and the zinc finger domain at its C-terminal region, respectively. In the present study, we examined the function of BCL-6 by using a recombinant adenovirus expressing BCL-6 (Ax1CA-BCL-6) and the lacZ reporter gene (Ax1CA-lacZ). Viability of CV-1 and HeLa cells infected with Ax1CA-BCL-6 was markedly reduced due to apoptosis, suggesting that BCL-6-overexpression induces apoptosis in CV-1 and HeLa cells. FACS analysis revealed that BCL-6-overexpressing cells are accumulated not only at the sub-G1 but also at G2/M phase. Induction of apoptosis by BCL-6 was preceded by down-regulation of apoptosis repressors BCL-2 and BCL-XL. These results suggest that BCL-6 induces apoptosis by regulating the expression of these apoptosis-regulating genes.
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页码:487 / 494
页数:7
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