Protein tyrosine kinase inhibitors prevent didemnin B‐induced apoptosis in HL‐60 cells

FEBS Letters

Alfons, Lawen¹  Vaillant, François¹  Johnson, Karina L.¹ 

[1] Department of Biochemistry and Molecular Biology, Monash University, Wellington Road, Clayton, VIC 3168, Australia

关键词: Apoptosis;    Didemnin B;    Tyrosine phosphorylation;    Tyrosine kinase inhibitor;   

DOI  :  10.1016/0014-5793(96)00203-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Didemnin B induces rapid apoptosis in human promyeloid HL-60 cells with an optimal concentration of 1 μM (Grubb et al. (1995) Biochem. Biophys. Res. Commun. 215, 1130–1136), but little is known about how it does so. In order to determine whether protein tyrosine phosphorylation is involved in this rapid induction of apoptosis, HL-60 cells were pre-treated with tyrosine kinase inhibitors for 1 h before didemnin B treatment. Genistein, 2,5-dihydroxycinnamic acid methyl ester, and a range of tyrphostins inhibit didemnin B-induced apoptotic morphology in a concentration-dependent manner. DNA fragmentation induced by didemnin B is also inhibited by genistein, 2,5-dihydroxycinnamic acid methyl ester, and tyrphostins.

【 授权许可】

Unknown