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Blood, 1 July 2002, Vol. 100, No. 1, pp. 96-106
HEMATOPOIESIS
Expression of the  4 integrin subunit induces monocytic
differentiation of 32D/v-Abl cells
Annarita Morena,
Sabrina Riccioni,
Alessandra Marchetti,
Alessandro Tartaglia Polcini,
Arthur M. Mercurio,
Giovanni Blandino,
Ada Sacchi, and
Rita Falcioni
From the Molecular Oncogenesis Laboratory, Regina Elena
Cancer Institute, Via delle Messi d'Oro, Rome, Italy; and the
Department of Pathology Research North, Beth Israel Deaconess Medical
Center and Harvard Medical School, Boston, MA.
The  6 4 integrin is the receptor for various laminin isoforms
and is a component of the hemidesmosome. Increased expression levels of
this integrin correlate with the aggressive phenotype of many
epithelial tumors compared with surrounding normal tissue. Furthermore,
the long cytoplasmic tail of the 4 integrin subunit has been
implicated in several signal transduction pathways that are involved
not only in invasion, but also in proliferation and apoptosis. Here we
report that the exogenous expression of 4 integrin in
32D/v-abl-transformed cells reduces tumor aggressiveness in vivo and strongly inhibits cell proliferation in vitro by inducing monocytic differentiation. These effects are accompanied by growth arrest and p73 protein accumulation. The hypothesis that the inhibition of v-Abl oncogenic capacity could allow the activation of the endogenous c-Abl was tested in RKO cells. The results clearly demonstrated a strong increase of c-Abl phosphorylation that is accompanied by its association with p73 protein. Overall, the reported
findings indicate that 64 integrin promotes growth arrest and
differentiation by modulating Abl kinases and p73 protein pathway(s).
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