The heat shock protein 90 inhibitor 17‐AAG induces cell cycle arrest and apoptosis in mantle cell lymphoma cell lines by depleting cyclin D1, Akt, Bid and activating …
GV Georgakis, Y Li, A Younes - British journal of haematology, 2006 - Wiley Online Library
GV Georgakis, Y Li, A Younes
British journal of haematology, 2006•Wiley Online LibraryMantle cell lymphoma (MCL), a distinct type of non‐Hodgkin lymphoma, is characterised by
the overexpression of cyclin D1. Heat shock protein 90 (HSP90) is a molecular chaperon to
proteins that regulate cell cycle and survival. 17‐allylamino‐17‐demethoxy‐geldanamycin
(17‐AAG), a HSP90 small molecule inhibitor, induced G0/1 cell cycle arrest and cell death in
a dose‐and time‐dependent manner in MCL cell lines. This effect was associated with the
downregulation of cyclin D1, cdk4 and Akt, depletion of Bid, and activation of the …
the overexpression of cyclin D1. Heat shock protein 90 (HSP90) is a molecular chaperon to
proteins that regulate cell cycle and survival. 17‐allylamino‐17‐demethoxy‐geldanamycin
(17‐AAG), a HSP90 small molecule inhibitor, induced G0/1 cell cycle arrest and cell death in
a dose‐and time‐dependent manner in MCL cell lines. This effect was associated with the
downregulation of cyclin D1, cdk4 and Akt, depletion of Bid, and activation of the …
Summary
Mantle cell lymphoma (MCL), a distinct type of non‐Hodgkin lymphoma, is characterised by the overexpression of cyclin D1. Heat shock protein 90 (HSP90) is a molecular chaperon to proteins that regulate cell cycle and survival. 17‐allylamino‐17‐demethoxy‐geldanamycin (17‐AAG), a HSP90 small molecule inhibitor, induced G0/1 cell cycle arrest and cell death in a dose‐ and time‐dependent manner in MCL cell lines. This effect was associated with the downregulation of cyclin D1, cdk4 and Akt, depletion of Bid, and activation of the intrinsic/mitochondrial caspase pathway. These data suggest that 17‐AAG may have a potential therapeutic value in patients with MCL.
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