NDLI: Down-regulation of achaete-scute complex homolog 1 (ASCL1) in neuroblastoma cells induces up-regulation of insulin-like growth factor 2 (IGF2)

Content Provider	Springer Nature Link
Author	Li, Jialing Neumann, Ingo Volkmer, Ines Staege, Martin Sebastian
Copyright Year	2010
Abstract	Neuroblastoma (NB) is the most common extra-cranial solid pediatric tumor. The prognosis of patients with NB has been improved during the last decades. However, treatment results for patients with advanced tumor stages are still unsatisfying. NB cells are characterized by a high tendency for spontaneous or induced differentiation. During differentiation, down-regulation of the basic helix-loop-helix transcription factor achaete-scute complex homolog 1 (ASCL1) has been observed but the consequences of ASCL1 down-regulation have not been elucidated. We used RNA interference to knock-down ASCL1 in NB cells. DNA microarray analysis was used for the identification of ASCL1-regulated genes. Furthermore, conventional and quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used for validation of ASCL1-regulated genes. Down-regulation of ASCL1 influenced the expression of several genes. After down-regulation of ASCL1, we observed very high expression of insulin-like growth factor 2 (IGF2), a factor that is known to be induced during differentiation of NB cells. RT-PCR indicated up-regulation of multiple IGF2 transcript variants after ASCL1 knock-down. Our data suggest that the ASCL1-pathway is responsible for the up-regulation of IGF2 during NB differentiation.
Starting Page	1515
Ending Page	1521
Page Count	7
File Format	PDF
ISSN	03014851
Journal	Molecular Biology Reports
Volume Number	38
Issue Number	3
e-ISSN	15734978
Language	English
Publisher	Springer Netherlands
Publisher Date	2010-09-15
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Neuroblastoma Gene expression Achaete-scute complex homolog 1 Insulin-like growth factor 2 Animal Biochemistry Animal Anatomy / Morphology / Histology
Content Type	Text
Resource Type	Article
Subject	Genetics Medicine Molecular Biology

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