Induction of apoptosis in leukemic cell lines treated with captopril, trandolapril and losartan: A new role in the treatment of leukaemia for these agents

• Published in: Leukemia research Vol. 33; no. 6; pp. 810 - 816
• Main Authors: De la Iglesia Iñigo, Silvia, López-Jorge, Carmen Elsa, Gómez-Casares, Maria Teresa, Lemes Castellano, Angelina, Martín Cabrera, Pedro, López Brito, Jezabel, Suárez Cabrera, Alexia, Molero Labarta, Teresa
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01-06-2009
• Subjects: ACE inhibitors; Angiotensin-Converting Enzyme Inhibitors - pharmacology; Apoptosis - drug effects; Blotting, Northern; Blotting, Western; Captopril - pharmacology; Cell Proliferation; Genes, myc; Hematology, Oncology and Palliative Medicine; HL60; Humans; Indoles - pharmacology; K562; K562 Cells; Leukemia cell lines; Leukemia, Erythroblastic, Acute - genetics; Leukemia, Erythroblastic, Acute - pathology; Losartan - pharmacology; Polymerase Chain Reaction; Renin–angiotensin system; Renin–angiotensin system; K562; ACE inhibitors; Leukemia cell lines; HL60
• ISSN: 0145-2126; 1873-5835
• DOI: 10.1016/j.leukres.2008.09.029

Abstract Renin–angiotensin system (RAS) in the bone marrow is related to proliferation and cellular differentiation. We investigated the effect of ACE inhibitors (ACEI) captopril (>1 mM) and trandolapril (>0.05 mM) and losartan (0.2 mM) on K562 cell line and K562 transfected with c-myc, bcl-x and bcl-2 (KmycB, Kbclx and Kbcl2 respectively). RAS components, proliferation, apoptosis and c-myc expression were analyzed. ACEI and losartan inhibited cell growth, decreased c-myc expression and increased apoptosis. These effects seem to be associated to angiotensin II-induced Smad activation. This work offers a new possible line of treatment for some acute myeloid leukemias and a new area of clinical research.