PT  - JOURNAL ARTICLE
AU  - YUKI OKUHASHI
AU  - MAI ITOH
AU  - SHUJI TOHDA
TI  - <em>GLI1</em> and <em>CTNNB1</em> Knockdown Activates NOTCH and mTOR Signalling in NB4 Myeloid Leukaemia Cells
AID  - 10.21873/anticanres.12990
DP  - 2018 Nov 01
TA  - Anticancer Research
PG  - 6329--6332
VI  - 38
IP  - 11
4099  - http://ar.iiarjournals.org/content/38/11/6329.short
4100  - http://ar.iiarjournals.org/content/38/11/6329.full
SO  - Anticancer Res2018 Nov 01; 38
AB  - 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 and Methods: 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.