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Leuk Res. 2017 Mar;54:1-6. doi: 10.1016/j.leukres.2016.12.005. Epub 2016 Dec 26.

Overexpression of PTP4A3 in ETV6-RUNX1 acute lymphoblastic leukemia.

Author information

1
Tampere Center for Child Health Research, University of Tampere and Tampere University Hospital, Tampere, Finland. Electronic address: toni.gronroos@staff.uta.fi.
2
Tampere Center for Child Health Research, University of Tampere and Tampere University Hospital, Tampere, Finland.
3
Institute of Biomedicine, School of Medicine, University of Eastern Finland, Kuopio, Finland.
4
Tampere Center for Child Health Research, University of Tampere and Tampere University Hospital, Tampere, Finland; Institute of Biosciences and Medical Technology, University of Tampere, Finland.
5
Institute of Biosciences and Medical Technology, University of Tampere, Finland; Department of Signal Processing, Tampere University of Technology, Tampere, Finland.

Abstract

Cell signalling, which is often derailed in cancer, is a network of multiple interconnected pathways with numerous feedback mechanisms. Dynamics of cell signalling is intimately regulated by addition and removal of phosphate groups by kinases and phosphatases. We examined expression of members of the PTP4A family of phosphatases across acute leukemias. While expression of PTP4A1 and PTP4A2 remained relatively unchanged across diseases, PTP4A3 showed marked overexpression in ETV6-RUNX1 and BCR-ABL1 subtypes of precursor B cell acute lymphoblastic leukemia. We show that PTP4A3 is regulated by the ETV6-RUNX1 fusion, but noticed no marked impact on cell viability either after PTP4A3 silencing or treatment with a PTP4A3 inhibitor. Regulation of PTP4A3 expression is altered in specific subgroups of acute leukemias and this is likely brought about by expression of the aberrant fusion genes.

KEYWORDS:

ETV6-RUNX1; Leukemia; PTP4A3

PMID:
28063378
DOI:
10.1016/j.leukres.2016.12.005
[Indexed for MEDLINE]

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