Article

CIP2A is over-expressed in acute myeloid leukaemia and associated with HL60 cells proliferation and differentiation.

Department of Haematology, Qilu Hospital of Shandong University, Jinan, China.
International journal of laboratory hematology (impact factor: 1.3). 01/2011; 33(3):290-8. DOI:10.1111/j.1751-553X.2010.01288.x pp.290-8
Source: PubMed

ABSTRACT CIP2A is a newly identified inhibitor of PP2A. It can stabilize c-Myc and promote anchorage-independent cell growth and tumour formation. CIP2A is over-expressed in some solid tumours although its expression in acute myeloid leukaemia (AML) is still unknown.
CIP2A mRNA and protein expressions were determined in bone marrow mononuclear cells of both patients with AML and healthy controls using reverse transcription polymerase chain reaction and Western blot, respectively. We used siRNA to knock-down CIP2A expression in HL60 cells and then examined its potential roles during the pathological progression of AML.
CIP2A mRNA was present in 54 of 70 (77.14%) patients with newly diagnosed AML and in 11 of 14 (70.86%) patients with relapsed AML, which was significantly higher than complete remission specimens and healthy controls (P<0.001). Knock-down of CIP2A in HL60 cells slowed down cell proliferation, decreased clonogenic activity and promoted cell differentiation.
These results suggest that CIP2A is over-expressed in patients with newly diagnosed/relapsed AML and the expression of CIP2A could have potential use as a clinical marker for AML relapse after treatment. The high expression of CIP2A in HL60 cells may be related to active cell proliferation and arrest of cell differentiation. This study may shed light on the molecular function of CIP2A in myeloid leukemogenesis.

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Keywords

active cell proliferation
 
acute myeloid leukaemia
 
AML relapse
 
anchorage-independent cell growth
 
bone marrow mononuclear cells
 
CIP2A mRNA
 
clinical marker
 
diagnosed/relapsed AML
 
HL60 cells
 
identified inhibitor
 
knock-down CIP2A expression
 
molecular function
 
myeloid leukemogenesis
 
pathological progression
 
potential roles
 
protein expressions
 
relapsed AML
 
reverse transcription polymerase chain reaction
 
solid tumours
 
tumour formation
 

J Wang