Targeted BIRC5 silencing using YM155 causes cell death in neuroblastoma cells with low ABCB1 expression
نویسندگان
چکیده
منابع مشابه
Targeted expression of MYCN causes neuroblastoma in transgenic mice.
The proto-oncogene MYCN is often amplified in human neuroblastomas. The assumption that the amplification contributes to tumorigenesis has never been tested directly. We have created transgenic mice that overexpress MYCN in neuroectodermal cells and develop neuroblastoma. Analysis of tumors by comparative genomic hybridization revealed gains and losses of at least seven chromosomal regions, all...
متن کاملKnockdown of survivin (BIRC5) causes apoptosis in neuroblastoma via mitotic catastrophe.
BIRC5 (survivin) is one of the genes located on chromosome arm 17q in the region that is often gained in neuroblastoma. BIRC5 is a protein in the intrinsic apoptotic pathway that interacts with XIAP and DIABLO leading to caspase-3 and caspase-9 inactivation. BIRC5 is also involved in stabilizing the microtubule-kinetochore dynamics. Based on the Affymetrix mRNA expression data, we here show tha...
متن کاملApoptotic Cell Death in Neuroblastoma
Neuroblastoma (NB) is one of the most common malignant solid tumors in childhood, which derives from the sympathoadrenal lineage of the neural crest and exhibits extremely heterogeneous biological and clinical behaviors. The infant patients frequently undergo spontaneous regression even with metastatic disease, whereas the patients of more than one year of age who suffer from disseminated disea...
متن کاملSilencing of survivin using YM155 induces apoptosis and chemosensitization in neuroblastomas cells.
OBJECTIVES Aggressive cell growth and chemoresistance are notorious obstacles in neuroblastoma therapy. Accumulating evidence suggests that survivin is preferentially expressed in cancer cells and plays a crucial role in cell division and apoptosis dysfunction. Thus, in the present study, we investigated whether silencing of survivin, using a novel small-molecule survivin suppressant, YM155 cou...
متن کاملExpression of truncated PrP targeted to Purkinje cells of PrP knockout mice causes Purkinje cell death and ataxia.
PrP knockout mice with disruption of only the PrP-encoding region (Zürich I-type) remain healthy, whereas mice with deletions extending upstream of the PrP-encoding exon (Nagasaki-type) suffer Purkinje cell loss and ataxia, associated with ectopic expression of Doppel in brain, particularly in Purkinje cells. The phenotype is abrogated by co-expression of full-length PrP. Doppel is 25% similar ...
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ژورنال
عنوان ژورنال: European Journal of Cancer
سال: 2012
ISSN: 0959-8049
DOI: 10.1016/j.ejca.2011.10.012