SNAIL is a key regulator of alveolar rhabdomyosarcoma tumor growth and differentiation through repression of MYF5 and MYOD function

Cell Death & Disease
Klaudia SkrzypekMarcin Majka

Abstract

Rhabdomyosarcoma (RMS) is a mesenchymal tumor of soft tissue in children that originates from a myogenic differentiation defect. Expression of SNAIL transcription factor is elevated in the alveolar subtype of RMS (ARMS), characterized by a low myogenic differentiation status and high aggressiveness. In RMS patients SNAIL level increases with higher stage. Moreover, SNAIL level negatively correlates with MYF5 expression. The differentiation of human ARMS cells diminishes SNAIL level. SNAIL silencing in ARMS cells inhibits proliferation and induces differentiation in vitro, and thereby completely abolishes the growth of human ARMS xenotransplants in vivo. SNAIL silencing induces myogenic differentiation by upregulation of myogenic factors and muscle-specific microRNAs, such as miR-206. SNAIL binds to the MYF5 promoter suppressing its expression. SNAIL displaces MYOD from E-box sequences (CANNTG) that are associated with genes expressed during differentiation and G/C rich in their central dinucleotides. SNAIL silencing allows the re-expression of MYF5 and canonical MYOD binding, promoting ARMS cell myogenic differentiation. In differentiating ARMS cells SNAIL forms repressive complex with histone deacetylates 1 and 2 (HDAC1/2) and...Continue Reading

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Citations

Jan 9, 2019·Nature Reviews. Disease Primers·Stephen X SkapekDouglas S Hawkins
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Datasets Mentioned

BETA
GSE92689

Methods Mentioned

BETA
transfection
ELISA
Chip
Assay
PCR
immunoprecipitation
Protein Assay
enzyme-linked immunosorbent assay
Co-IP
Fluorescence

Software Mentioned

cellSens Dimension
affy package
Bioconductor
GraphPad Prism
R
ConSite
ImageJ

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