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Phosphoinositide 3-kinase/Akt involvement in arsenic trioxide resistance of human leukemia cells by Giovanna Tabellini; Alessandra Cappellini; Pier Luigi Tazzari; Federica Falà; Anna Maria Billi; Lucia Manzoli; Lucio Cocco; Alberto M. Martelli is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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## Abstract The purpose of this study was to evaluate the possible involvement of the phosphoinositide 3‐kinase (PI3K)/Akt survival pathway in determining resistance to arsenic trioxide (As~2~O~3~)‐induced apoptosis. We employed a HL60 cell clone (HL60AR) with a constitutively active PI3K/Akt survival pathway, as well as U937 and K562 cells. In addition, we used parental (PT) HL60 cells overexpressing a constitutively active Akt. Selective pharmacological inhibitors of the PI3K/Akt axis (LY294002, wortmannin) were employed to influence the sensitivity to As~2~O~3~. While HL60PT cells were sensitive to 2.5 μM As~2~O~3~ and died of apoptosis, HL60AR cells were resistant up to 5 μM As~2~O~3~. Treatment with either LY294002 or wortmannin lowered resistance of HL60AR cells to As~2~O~3~. Also in U937 and K562 cells, inhibitors of the PI3K/Akt axis caused a decrease in As~2~O~3~ resistance. Overexpression of constitutively active Akt in HL60PT cells caused the induction of resistance to 2.5 μM As~2~O~3~. Conversely, forced expression of a dominant negative Akt in HL60AR cells resulted in a decrease in As~2~O~3~ resistance. Moreover, HL60 cell resistance to 2.5 μM As~2~O~3~ could be signif

Who reads Phosphoinositide 3-kinase/Akt involvement in arsenic trioxide resistance of human leukemia cells?

Author

Giovanna Tabellini; Alessandra Cappellini; Pier Luigi Tazzari; Federica Falà; Anna Maria Billi; Lucia Manzoli; Lucio Cocco; Alberto M. Martelli

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0021-9541)

Published

2004

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)