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miR-34b/miR-34c: a regulator of TCL1 expression in 11q− chronic lymphocytic leukaemia?

Leukemia volume 23, pages 2174–2177 (2009)Cite this article

TCL1 (T-cell leukaemia/lymphoma 1) is a 114-amino-acid protein normally expressed in CD3−CD4−CD8− thymic precursors, some dendritic cells and developing B cells. In B cells, TCL1 exerts indirect transcriptional effects through (i) an association with c-Jun, JunB and c-Fos, which results in the inhibition of AP-1-dependent transcription and (ii) by interacting with the nuclear factor-κB coactivator p300/CREB-binding protein. This leads to an activation of the nuclear factor-κB-dependent transcriptional programme, and to the inhibition of cell death.1

TCL1 is overexpressed in most cases of chronic lymphocytic leukaemias (CLLs).2 Several studies have delineated the links existing between overexpression of TCL1 in CLL and some specific chromosomal abnormalities. Expression of TCL1 in CLL samples varied from complete absence to strong expression, and was dependent of the immunophenotypic and molecular CLL subgroups.2 Cases that strongly expressed TCL1 were more frequently found in cohorts having either (i) higher expression levels of ZAP70, (ii) unmutated IgVH genes and/or (iii) loss or monosomy of the 11q22/ATM locus. A correlation between the high expression of TCL1 and 11q deletion was also described by Pekarsky et al.,3 who showed that a high expression of TCL1 was frequently observed, whereas a low expression was very rare in aggressive CLLs with 11q deletions (11q−) (24 out of 32 and 1 case out of 32, respectively). Taken together, these results suggest that the overexpression of TCL1 in CLL can be linked with a deletion of 11q. The mechanisms underlying TCL1 overexpression in B-cell pathologies, especially in 11q− CLL, are poorly understood.

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Acknowledgements

We thank Dr HP Koeffler (Cedars-Sinai Medical Center, University of California at Los Angeles School of Medecine, Los Angeles, California) for helpful comments. This work was supported by the Institut National du Cancer (PL0079), and the European Community (MICROENVIMET, FP7-HEALTH-F2-2008-201279). We acknowledge the excellent support of the Nice-Sophia Antipolis Transcriptome Platform of the Marseille-Nice Genopole for the microarray experiments. We also thank Franck Aguila for artwork.

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  1. S Raynaud and P Barbry: These authors contributed equally to the work.

Authors and Affiliations

  1. CNRS, IPMC, UMR6097, Sophia Antipolis, France

    B Cardinaud, B Marcet, K Robbe-Sermesant, K LeBrigand, B Mari & P Barbry

  2. Université de Nice Sophia-Antipolis, IPMC, UMR6097, Sophia Antipolis, France

    B Cardinaud, B Marcet, K Robbe-Sermesant, K LeBrigand, B Mari & P Barbry

  3. CHU de Nice, Laboratoire d'oncohématologie, Hôpital, Pasteur, Nice, France

    C Moreilhon & S Raynaud

  4. Hôpital Avicenne, Université Paris XIII, Laboratoire d'hématologie, Bobigny, France

    V Eclache & F Cymbalista

  5. Université Victor Segalen Bordeaux 2, EA 4135, Bordeaux, France E-mail: barbry@ipmc.cnrs.fr,

    B Cardinaud

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Cardinaud, B., Moreilhon, C., Marcet, B. et al. miR-34b/miR-34c: a regulator of TCL1 expression in 11q− chronic lymphocytic leukaemia?. Leukemia 23, 2174–2177 (2009). https://doi.org/10.1038/leu.2009.125

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