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Co‐ordinated downregulation of bcl‐2 and bax expression during granulocytic and macrophage‐like differentiation of the HL60 promyelocytic leukaemia cell line
Author(s) -
Mengubas Kamuran,
Riordan Fiona A.,
Victor Hoffbrand A.,
Gitendra Wickremasinghe R.
Publication year - 1996
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(96)00983-0
Subject(s) - downregulation and upregulation , hl60 , retinoic acid , apoptosis , bax protein , microbiology and biotechnology , cellular differentiation , myeloid , cell culture , chemistry , phorbol , biology , cancer research , protein expression , biochemistry , signal transduction , gene , protein kinase c , genetics
The bcl‐2 protein suppresses apoptosis and the bax protein opposes the cytoprotective effect of bcl‐2. A decrease in bcl‐2 levels has been implicated in the induction of apoptosis during the terminal differentiation of HL60 myeloid leukaemia cells. We show here that bax protein also declined with a time course similar to the downregulation of bcl‐2 following treatment of HL60 with phorbol myristate acetate (PMA), dimethyl sulphoxide (DMSO) or retinoic acid (RA). Decreased bcl‐2 protein expression in induced cells was associated with down‐regulation of its mRNA. By contrast, the decrease in bax occurred by a post‐transcriptional mechanism. Co‐ordinate downregulation of bcl‐2 and bax proteins may fine‐tune the induction of apoptosis during cellular differentiation.