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 Blood, 15 December 2007, Vol. 110, No. 13, pp. 4406-4416.
Prepublished online as a Blood First Edition Paper on September 10, 2007; DOI 10.1182/blood-2006-11-059501.

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NEOPLASIA

The TCL1 oncoprotein inhibits activation-induced cell death by impairing PKC{theta} and ERK pathways

Gilles Despouy1,2, Marjorie Joiner1,2, Emilie Le Toriellec1,2, Robert Weil3, and Marc Henri Stern1,2

1 Institut Curie, Centre de Recherche, Paris; 2 Inserm U830, Paris; and 3 Centre National de la Recherche Scientifique (CNRS) URA2582, Institut Pasteur, Paris, France

The TCL1/MTCP1 oncogenes were identified on the basis of their involvement in T-cell prolymphocytic leukemia (T-PLL). TCL1 and MTCP1 proteins directly interact with AKT and modulate the AKT signal-transduction pathway, but the relevance of this mechanism in leukemogenesis remains unclear. We investigate the biologic functions of TCL1 in the T-cell lineage using various cell lines, and primary malignant and normal lymphocytes. In the Jurkat cell line, expression of TCL1 had no effect in unstimulated cells, whereas it abrogated activation-induced cell death (AICD). These cellular effects were concomitant with a major inhibition by TCL1 of PKC{theta} and ERK pathways. Secondly, the TCL1-driven T-cell leukemia cell line SUP-T11 was shown to have impaired PKC{theta} and ERK phosphorylation upon stimulation, which were restored by TCL1 inhibition using RNA interference. Finally, defects in these pathways were also observed in primary malignant (T-PLL) and transduced normal T lymphocytes expressing TCL1. Altogether, our data demonstrated that TCL1 inhibits AICD in T cells by blocking PKC{theta} and ERK activation, upon cellular activation.


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E. Le Toriellec, G. Despouy, G. Pierron, N. Gaye, M. Joiner, D. Bellanger, A. Vincent-Salomon, and M.-H. Stern
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