Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/94898
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Type: Journal article
Title: BCR-ABL1 tyrosine kinase sustained MECOM expression in chronic myeloid leukaemia
Author: Roy, S.
Jørgensen, H.
Roy, P.
Abed El Baky, M.
Melo, J.
Strathdee, G.
Holyoake, T.
Bartholomew, C.
Citation: British Journal of Haematology, 2012; 157(4):446-456
Publisher: Blackwell Publishing
Issue Date: 2012
ISSN: 0007-1048
1365-2141
Statement of
Responsibility: 
Swagata Roy, Heather G. Jørgensen, Poornima Roy, Mohamed Abed El Baky, Junia V. Melo, Gordon Strathdee, Tessa L. Holyoake, and Chris Bartholomew
Abstract: MECOM oncogene expression correlates with chronic myeloid leukaemia (CML) progression. Here we show that the knockdown of MECOM (E) and MECOM (ME) isoforms reduces cell division at low cell density, inhibits colony-forming cells by 34% and moderately reduces BCR-ABL1 mRNA and protein expression but not tyrosine kinase catalytic activity in K562 cells. We also show that both E and ME are expressed in CD34(+) selected cells of both CML chronic phase (CML-CP), and non-CML (normal) origin. Furthermore, MECOM mRNA and protein expression were repressed by imatinib mesylate treatment of CML-CP CD34(+) cells, K562 and KY01 cell lines whereas imatinib had no effect in non-CML BCR-ABL1 -ve CD34(+) cells. Together these results suggest that BCR-ABL1 tyrosine kinase catalytic activity regulates MECOM gene expression in CML-CP progenitor cells and that the BCR-ABL1 oncoprotein partially mediates its biological activity through MECOM. MECOM gene expression in CML-CP progenitor cells would provide an in vivo selective advantage, contributing to CML pathogenesis.
Keywords: MECOM
BCR-ABL1
tyrosine kinase
imatinib
chronic myeloid leukaemia
Rights: © 2012 Blackwell Publishing Ltd
DOI: 10.1111/j.1365-2141.2012.09078.x
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