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Cancer Cell death Cell cycle Cytoskeleton Exo/endocytosis Differentiation Division Organelles Signalling Stem cells Trafficking
Cell Biology International (2006) 30, 727–732 (Printed in Great Britain)
CD38 expression enhances sensitivity of lymphoma T and B cell lines to biochemical and receptor-mediated apoptosis
Armando Gregorinia*, Marco Tomasettib, Cristina Cintib, Daniela Colombac and Stella Colombad
aIstituto di Psicologia “L. Meschieri”, Università di Urbino “Carlo Bo”, via O. Ubaldini 17, 61029 Urbino (PU), Italy
bDipartimento di Patologia Molecolare e Terapie Innovative, Università Politecnica delle Marche, via Brecce Bianche, 60131 Ancona, Italy
cIstituto di Clinica Medica I, Università di Palermo, P.zza delle Cliniche 2, 90127 Palermo, Italy
dIstituto di Ecologia e Biologia Ambientale, Università di Urbino “Carlo Bo”, Via I. Maggetti 22, 61029 Urbino (PU), Italy


Abstract

CD38 has been widely characterised both as an ectoenzyme and as a receptor. In the present paper, we investigated the role of CD38 as possible modulator of apoptosis. CD38-positive (CD38+) and negative (CD38) fractions, obtained by sorting CD38+ cells from lymphoma T (Jurkat) and lymphoma B (Raji) and by transfecting lymphoma LG14 and myeloid leukemia K562 cell lines, were used. Cellular subpopulations were exposed to different triggers (H2O2, UV-B, α-TOS and hrTRAIL) and the extent of apoptosis was determined by Annexin V-FITC/PI assay. Our data showed that, in lymphoma cells, propensity to apoptosis was significantly linked to CD38 expression and that, remarkably, such response was independent of the nature of the trigger used. Inhibition of CD38 expression by antisense oligonucleotides treatment resulted in CD38-silenced fractions which were as prone to apoptosis as CD38 ones. Notably, susceptibility of K562 to apoptosis-inducing challenges was not affected by CD38 expression.


Key words: CD38, Apoptosis, Lymphoma T cells, Lymphoma B cells, Myeloid leukemia cells.

*Corresponding author. Tel.: +39 722 303438; fax: +39 722 303436.


Received 15 February 2006/11 April 2006; accepted 10 May 2006

doi:10.1016/j.cellbi.2006.05.004


ISSN Print: 1065-6995
ISSN Electronic: 1095-8355
Published by Portland Press Limited on behalf of the International Federation for Cell Biology (IFCB)