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Prepublished online as a Blood First Edition Paper on September 19, 2002; DOI 10.1182/blood-2002-05-1519.
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Blood, 1 February 2003, Vol. 101, No. 3, pp. 1118-1127
NEOPLASIA
Temporal gene expression profile of human precursor B
leukemia cells induced by adhesion receptor: identification of pathways
regulating B-cell survival
Anne Laurence Astier,
Ronghui Xu,
Marek Svoboda,
Esther Hinds,
Olivier Munoz,
Rosalie de
Beaumont,
Colin Daniel Crean,
Theodore Gabig, and
Arnold Stephen Freedman
From the Department of Adult Oncology, Dana-Farber
Cancer Institute, Boston, MA; the Department of Biostatistical Science,
Harvard School of Public Health, Dana-Farber Cancer Institute, Boston,
MA; the Department of Medicine, Harvard Medical School, Boston, MA; the
Department of Medicine, Indiana University School of Medicine,
Indianapolis; and the Biomedical Research Institute, Long Island Jewish
Health System, Manhasset, NY.
The physical interactions between B cells and stromal cells from
the lymphoid tissue microenvironment are critical to the survival of
normal and malignant B cells. They are principally mediated by
integrins expressed on B cells and counterreceptors on stromal
cells. Specifically,  4 1 integrin engagement rescues B cells from
physiological or drug-induced apoptosis. Therefore, in order to
understand the mechanisms by which integrins prevent apoptosis in
leukemia B cells, we compared the temporal gene expression profiles
induced by 1-integrin ligation with fibronectin (Fn) or adhesion by
poly-L-Lysine in serum-starved precursor B leukemia cells. Among the 38 selected differentially expressed genes, 6 genes involved in adhesion
(VAV2, EPB41L1, CORO1A), proliferation (FRAP1,
CCT4), and intercellular communication (GJB3) were
validated by real-time quantitative polymerase chain reaction
(RT-Q-PCR). Gene expression modulation could also be validated at the
protein level for 5 other genes. We show that integrin stimulation
up-regulated FBI-1 expression but inhibited CD79a, Requiem,
c-Fos, and caspase 7 induction when the cells underwent apoptosis. We
further demonstrate that Fn stimulation also inhibits caspase 3 activation but increases XIAP and survivin expression.
Moreover, integrin stimulation also prevents caspase activation induced
by doxorubicin. Therefore, we identified genes modulated by adhesion of
human precursor B leukemia cells that regulate proliferation and
apoptosis, highlighting new pathways that might provide insights into
future therapy aiming at targeting apoptosis of leukemia cells.
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