TAILIEUCHUNG - Báo cáo khoa học: Sp1-like sequences mediate human caspase-3 promoter activation by p73 and cisplatin

Caspase-3 is a cysteine protease that plays a central role in the execution of apoptosis induced by a wide variety of stimuli. However, little is known about the mechanisms involved in the regulation of caspase-3 gene tran-scription. | ễFEBS Journal Sp1-like sequences mediate human caspase-3 promoter activation by p73 and cisplatin Cherukuri Sudhakar Nishant Jain and Ghanshyam Swarup Centre for Cellular and Molecular Biology Hyderabad India Keywords caspase-3 cisplatin p73 promoter activation Sp1 Correspondence G. Swarup Centre for Cellular and Molecular Biology UppalRoad Hyderabad 500 007 India Fax 91 40 27160591 or 91 40 27160311 Tel 91 40 27192616 or 91 40 27160222 E-mail gshyam@ Received 16 October 2007 revised 22 February 2008 accepted 3 March 2008 doi Caspase-3 is a cysteine protease that plays a central role in the execution of apoptosis induced by a wide variety of stimuli. However little is known about the mechanisms involved in the regulation of caspase-3 gene transcription. This study was carried out to characterize the human caspase-3 promoter and to understand the mechanisms involved in the induction of caspase-3 gene expression in response to the anticancer drug cisplatin and p73. Caspase-3 gene expression was induced by treatment of cells with cisplatin which also induced p73 protein in HeLa and K562 cells. The human caspase-3 promoter was cloned and characterized. p73b strongly activated the caspase-3 promoter whereas p73a showed less activation. Cisplatin treatment increased caspase-3 promoter activity. Basal and cisplatin-induced promoter activity was inhibited by the p73 inhibitor p73DD. Deletion analysis defined a minimal promoter of 120 base pairs which showed good basal and p73b-induced activity. The examination of the minimal promoter sequence showed several putative Sp1 sites but no p53 p73 site. The caspase-3 promoter was activated by Sp1 in Sp1-deficient Drosophila SL-2 cells. Sp1-induced promoter activity was further enhanced by p73b in SL-2 cells. Mutation of Sp1 sites in the minimal promoter resulted in a loss of basal and p73-induced promoter activity. These results show that caspase-3 gene transcription is induced by .

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