KCTD15 is overexpressed in human childhood B-cell acute lymphoid leukemia

Giovanni Smaldone, Giuliana Beneduce, Mariarosaria Incoronato, Katia Pane, Monica Franzese, Luigi Coppola, Angela Cordella, Rosanna Parasole, Mimmo Ripaldi, Giovanni Nassa, Andrea Soricelli, Luigi Vitagliano, Peppino Mirabelli, Marco Salvatore

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Leukemic cells originate from the malignant transformation of undifferentiated myeloid/lymphoid hematopoietic progenitors normally residing in bone marrow. As the precise molecular mechanisms underlying this heterogeneous disease are yet to be disclosed, the identification and the validation of novel actors in leukemia is of extreme importance. Here, we show that KCTD15, a member of the emerging class of KCTD ((K)potassium Channel Tetramerization Domain containing) proteins, is strongly upregulated in patients affected by B-cell type acute lymphoblastic leukemia (B-ALL) and in continuous cell lines (RS4;11, REH, TOM-1, SEM) derived from this form of childhood leukemia. Interestingly, KCTD15 downregulation induces apoptosis and cell death suggesting that it has a role in cellular homeostasis and proliferation. In addition, stimulation of normal lymphocytes with the pokeweed mitogen leads to increased KCTD15 levels in a fashion comparable to those observed in proliferating leukemic cells. In this way, the role of KCTD15 is likely not confined to the B-ALL pathological state and extends to activation and proliferation of normal lymphocytes. Collectively, data here presented indicate that KCTD15 is an important and hitherto unidentified player in childhood lymphoid leukemia, and its study could open a new scenario for the identification of altered and still unknown molecular pathways in leukemia.

Original languageEnglish
Article number20108
JournalScientific Reports
Issue number1
Publication statusPublished - Dec 1 2019

ASJC Scopus subject areas

  • General


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