GLI1 and CTNNB1 Knockdown Activates NOTCH and mTOR Signalling in NB4 Myeloid Leukaemia Cells.
Anticancer Res
; 38(11): 6329-6332, 2018 Nov.
Article
em En
| MEDLINE
| ID: mdl-30396954
ABSTRACT
BACKGROUND:
Hedgehog (HH), WNT, NOTCH, and mechanistic target of rapamycin (mTOR) signalling pathways are known to regulate the progression of cancer; however, their interaction in leukaemia cells is not fully clarified. MATERIALS ANDMETHODS:
Myeloid and T-lymphoblastic leukaemia cell lines (NB4, THP-1, Jurkat, and DND-41) were transfected with small interfering RNAs targeting the glioma-associated oncogene homolog 1 (GLI1) and catenin beta-1 (CTNNB1) genes involved in the regulation of HH and WNT pathways, respectively, and we examined cell proliferation and gene expression.RESULTS:
The knockdown of GLI1 and CTNNB1 did not significantly affect proliferation of any cell line; however, it up-regulated the expression of NOTCH1, cleaved NOTCH1 fragment, and phosphorylated mTOR in NB4 cells, but not in the other cell lines.CONCLUSION:
Our data suggest that HH and WNT act upstream of NOTCH and mTOR pathways and negatively regulate them in myeloid NB4 cells. Further studies are required to determine the biological significance of this signalling crosstalk in leukaemia.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Leucemia Mieloide Aguda
/
Beta Catenina
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Receptor Notch1
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Serina-Treonina Quinases TOR
/
Proteína GLI1 em Dedos de Zinco
Limite:
Humans
Idioma:
En
Revista:
Anticancer Res
Ano de publicação:
2018
Tipo de documento:
Article