Silencing of the microtubule-associated proteins doublecortin-like and doublecortin-like kinase-long induces apoptosis in neuroblastoma cells

Carla S. Verissimo, Jan J. Molenaar, John Meerman, Jordi Carreras Puigvert, Fieke Lamers, Jan Koster, Erik H.J. Danen, Bob Van De Water, Rogier Versteeg, Carlos P. Fitzsimons, Erno Vreugdenhil

Research output: Contribution to journalArticlepeer-review

32 Citations (Scopus)

Abstract

Doublecortin-like kinase-long (DCLK-long) and doublecortin-like (DCL) are two splice variants of DCLK gene. DCL and DCLK-long are microtubule-associated proteins with specific expression in proliferative neural progenitor cells. We have tested the hypothesis that knockdown of DCL/DCLK-long by RNA interference technology will induce cell death in neuroblastoma (NB) cells. First, we analyzed the expression of DCL and DCLK-long in several human neuroblastic tumors, other tumors, and normal tissues, revealing high expression of both DCL and DCLK-long in NB and glioma. Secondly, gene expression profiling revealed numerous differentially expressed genes indicating apoptosis induction after DCL/DCLK-long knockdown in NB cells. Finally, apoptosis was confirmed by time-lapse imaging of phosphatidylserine translocation, caspase-3 activation, live/dead double staining assays, and fluorescence-activated cell sorting. Together, our results suggest that silencing DCL/DCLK-long induces apoptosis in NB cells.

Original languageEnglish
Pages (from-to)399-414
Number of pages16
JournalEndocrine-Related Cancer
Volume17
Issue number2
DOIs
Publication statusPublished - Jun 2010
Externally publishedYes

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