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

Publication Type:

Journal Article

Source:

Endocr Relat Cancer, Volume 17, Number 2, p.399-414 (2010)

DOI Name (links to online publication)

10.1677/ERC-09-0301

Keywords:

ACTIVATION; Apoptosis; Caspase 3; CELL; Cell Death; CELLS; DCLK; EXPRESSION; expression profiling; GENE; Gene Expression; Gene Expression Profiling; GENE-EXPRESSION; Genes; Glioma; Human; INDUCTION; interference; MICROTUBULE-ASSOCIATED PROTEIN; Microtubul

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

18/01/2013