当前位置： SCI文献检索 > BRITISH JOURNAL OF CANCER期刊下所有文献 > Stable interference of EWS-FLI1 in an Ewing sarcoma cell line impairs IGF-1/IGF-1R signalling and reveals TOPK as a new target.

Stable interference of EWS-FLI1 in an Ewing sarcoma cell line impairs IGF-1/IGF-1R signalling and reveals TOPK as a new target.

Abstract：

BACKGROUND:Ewing sarcoma is a paradigm of solid tumour -bearing chromosomal translocations resulting in fusion proteins that act as deregulated transcription factors. Ewing sarcoma translocations fuse the EWS gene with an ETS transcription factor, mainly FLI1. Most of the EWS-FLI1 target genes still remain unknown and many have been identified in heterologous model systems. METHODS:We have developed a stable RNA interference model knocking down EWS-FLI1 in the Ewing sarcoma cell line TC71. Gene expression analyses were performed to study the effect of RNA interference on the genetic signature of EWS-FLI1 and to identify genes that could contribute to tumourigenesis. RESULTS:EWS-FLI1 inhibition induced apoptosis, reduced cell migratory and tumourigenic capacities, and caused reduction in tumour growth. IGF-1 was downregulated and the IGF-1/IGF-1R signalling pathway was impaired. PBK/TOPK (T-LAK cell-originated protein kinase) expression was decreased because of EWS-FLI1 inhibition. We showed that TOPK is a new target gene of EWS-FLI1. TOPK inhibition prompted a decrease in the proliferation rate and a dramatic change in the cell's ability to grow in coalescence. CONCLUSION:This is the first report of TOPK activity in Ewing sarcoma and suggests a significant role of this MAPKK-like protein kinase in the Ewing sarcoma biology.

journal_name

Br J Cancer

journal_title

British journal of cancer

authors

Herrero-Martín D,Osuna D,Ordóñez JL,Sevillano V,Martins AS,Mackintosh C,Campos M,Madoz-Gúrpide J,Otero-Motta AP,Caballero G,Amaral AT,Wai DH,Braun Y,Eisenacher M,Schaefer KL,Poremba C,de Alava E

doi

10.1038/sj.bjc.6605104

subject

Has Abstract

pub_date

2009-07-07 00:00:00

pages

80-90

issue

1

eissn

0007-0920

issn

1532-1827

pii

6605104

journal_volume

101

pub_type

杂志文章

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