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:58
作者
Yamochi, T
Kaneita, Y
Akiyama, T
Mori, S
Moriyama, M
机构
[1] Univ Tokyo, Inst Med Sci, Dept Pathol, Minato Ku, Tokyo 108, Japan
[2] Osaka Univ, Microbial Dis Res Inst, Dept Oncogene Res, Suita, Osaka 565, Japan
关键词
BCL-6; apoptosis; cell cycle; BCL-2; recombinant adenovirus;
D O I
10.1038/sj.onc.1202334
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
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. FAGS 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-X-L. These results suggest that BCL-6 induces apoptosis by regulating the expression of these apoptosis-regulating genes.
引用
收藏
页码:487 / 494
页数:8
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