Detailed Information on Publication Record
2015
The Expression of c-Myb Correlates with the Levels of Rhabdomyosarcoma-specific Marker Myogenin
KASPAR, Petr, Martina ZIKOVA, Petr BARTUNEK, Jaroslav ŠTĚRBA, Hynek STRNAD et. al.Basic information
Original name
The Expression of c-Myb Correlates with the Levels of Rhabdomyosarcoma-specific Marker Myogenin
Authors
KASPAR, Petr (203 Czech Republic, guarantor), Martina ZIKOVA (203 Czech Republic), Petr BARTUNEK (203 Czech Republic), Jaroslav ŠTĚRBA (203 Czech Republic, belonging to the institution), Hynek STRNAD (203 Czech Republic), Leoš KŘEN (203 Czech Republic, belonging to the institution) and Radislav SEDLACEK (203 Czech Republic)
Edition
Scientific Reports, London, Nature Publishing Group, 2015, 2045-2322
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
Genetics and molecular biology
Country of publisher
United Kingdom of Great Britain and Northern Ireland
Confidentiality degree
není předmětem státního či obchodního tajemství
Impact factor
Impact factor: 5.228
RIV identification code
RIV/00216224:14110/15:00085064
Organization unit
Faculty of Medicine
UT WoS
000362718600003
Keywords in English
CELL-DIFFERENTIATION; PEDIATRIC RHABDOMYOSARCOMAS; GENE-EXPRESSION; DOWN-REGULATION; CANCER-CELLS; PROLIFERATION; MICRORNAS; SURVIVAL; LEUKEMIA; INVASION
Tags
Tags
International impact, Reviewed
Změněno: 3/12/2015 16:00, Soňa Böhmová
Abstract
V originále
The transcription factor c-Myb is required for modulation of progenitor cells in several tissues, including skeletal muscle and its upregulation is observed in many human malignancies. Rhabdomyosarcomas (RMS) are a heterogeneous group of mesodermal tumors with features of developing skeletal muscle. Several miRNAs are downregulated in RMS, including miR-150, a negative regulator of c-Myb expression. Using the C2C12 myoblast cell line, a cellular model of skeletal muscle differentiation, we showed that miR-150 controls c-Myb expression mainly at the level of translation. We hypothesized that a similar mechanism of c-Myb regulation operates in RMS tumors. We examined expression of c-Myb by immunohistochemistry and revealed c-Myb positivity in alveolar and embryonal tumors, the two most common subgroups of RMS. Furthermore, we showed direct correlation between c-Myb production and myogenin expression. Interestingly, high myogenin levels indicate poor prognosis in RMS patients. c-Myb could, therefore, contribute to the tumor phenotype by executing its inhibitory role in skeletal muscle differentiation. We also showed that c-Myb protein is abundant in migratory C2C12 myoblasts and its ectopic expression potentiates cell motility. In summary, our results implicate that metastatic properties of some RMS subtypes might be linked to c-Myb function.