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.Základní údaje
Originální název
The Expression of c-Myb Correlates with the Levels of Rhabdomyosarcoma-specific Marker Myogenin
Autoři
KASPAR, Petr (203 Česká republika, garant), Martina ZIKOVA (203 Česká republika), Petr BARTUNEK (203 Česká republika), Jaroslav ŠTĚRBA (203 Česká republika, domácí), Hynek STRNAD (203 Česká republika), Leoš KŘEN (203 Česká republika, domácí) a Radislav SEDLACEK (203 Česká republika)
Vydání
Scientific Reports, London, Nature Publishing Group, 2015, 2045-2322
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
Genetika a molekulární biologie
Stát vydavatele
Velká Británie a Severní Irsko
Utajení
není předmětem státního či obchodního tajemství
Impakt faktor
Impact factor: 5.228
Kód RIV
RIV/00216224:14110/15:00085064
Organizační jednotka
Lékařská fakulta
UT WoS
000362718600003
Klíčová slova anglicky
CELL-DIFFERENTIATION; PEDIATRIC RHABDOMYOSARCOMAS; GENE-EXPRESSION; DOWN-REGULATION; CANCER-CELLS; PROLIFERATION; MICRORNAS; SURVIVAL; LEUKEMIA; INVASION
Štítky
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 3. 12. 2015 16:00, Soňa Böhmová
Anotace
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.