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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

Abstract

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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Acknowledgements

We thank to Dr Junichiro Inoue for provision of bcl-XL cDNA and also thank to Dr Yoshihide Tsujimoto for provision of bcl-2 cDNA. We thank to Dr Masao Seto for provision of plasmid DNA containing 5′-flanking region of bcl-2 gene. We thank to Dr Izum Saito for helpful suggestions and discussion on generating the recombinant adenoviruses, and also thank to him for provision of pAdex1CAwt cassette cosmid DNA.

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Yamochi, T., Kaneita, Y., Akiyama, T. et al. 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. Oncogene 18, 487–494 (1999). https://doi.org/10.1038/sj.onc.1202334

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