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Cellular and Molecular Biology 42: Apoptosis Regulators 3

BH3 α-helical proteomimetics inhibits Bcl-XL/Bax interaction and induce apoptosis in human cancer cells

Aslamussaman Kazi, Hang Yin, Hong-Gang Wang, Andrew D. Hamilton and Said M. Sebti
Aslamussaman Kazi
H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL and Yale University, New Haven, CT
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Hang Yin
H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL and Yale University, New Haven, CT
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Hong-Gang Wang
H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL and Yale University, New Haven, CT
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Andrew D. Hamilton
H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL and Yale University, New Haven, CT
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Said M. Sebti
H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL and Yale University, New Haven, CT
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DOI:  Published May 2005
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Proc Amer Assoc Cancer Res, Volume 46, 2005

Abstract

3512

One mechanism by which tumors either die or survive is thought to depend at least in part on the interaction between prosurvival (i.e. Bcl-2, Bcl-XL) and proapoptotic (i.e. Bax, Bak) proteins. The BH3 domain is the α-helical region of the pro-apoptotic proteins that binds to the prosurvival proteins. We have designed BH3 α-helical mimics with the ultimate goal of displacing Bcl2- and Bcl-XL-bound proapoptotic proteins and inducing tumor cell death. One of these, BH3M-6 is a non-peptide terphenyl that spacially projects side chains in a similar manner to that of the three turns of the BH3 α-helix of Bax. Using fluorescence polarization and GST-pulldown assays we showed that BH3M-6 disrupted the association of Bcl-XL with Bak and Bax, respectively. Furthermore, in intact human lung cancer A-549 cells, BH3M-6 inhibited proliferation and tumor cell survival as meeasured by MTT, soft agar and trypan blue assays. Finally, BH3M-6 induced apoptosis as demonstrated by DAPI staining, Tunel, cytochrome c release, caspase 3 activation and PARP-cleavage assays. Taken together these results show that small, non-peptidic synthetic mimics of the α-helical BH3 domain are able to inhibit the association of Bcl-XL with Bak and Bax and induce apoptosis in human cancer cells.

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Cancer Research: 65 (9 Supplement)
May 2005
Volume 65, Issue 9 Supplement
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BH3 α-helical proteomimetics inhibits Bcl-XL/Bax interaction and induce apoptosis in human cancer cells
Aslamussaman Kazi, Hang Yin, Hong-Gang Wang, Andrew D. Hamilton and Said M. Sebti
Cancer Res May 1 2005 (65) (9 Supplement) 827;

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BH3 α-helical proteomimetics inhibits Bcl-XL/Bax interaction and induce apoptosis in human cancer cells
Aslamussaman Kazi, Hang Yin, Hong-Gang Wang, Andrew D. Hamilton and Said M. Sebti
Cancer Res May 1 2005 (65) (9 Supplement) 827;
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Cancer Research Online ISSN: 1538-7445
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