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Annexin II cell surface and mRNA expression in human acute myeloid leukaemia cell lines
Shane A Olwill1, Hugh McGlynn, William S Gilmore
1School of Biomedical Sciences, University of Ulster, Coleraine BT52 1SA Northern Ireland, UK. shane.olwill@fusionantibodies.com
Introduction:
Acute promyelocytic leukaemia (APL) (M3) is associated with both a characteristic t(15;17) and severe bleeding diathesis caused by disseminated intravascular coagulation (DIC) and/or hyperfibrinolysis. It has been suggested that annexin II, a coreceptor for tissue plasminogen activator (t-PA) and plasminogen (PLG), is overexpressed on the surface of promyelocytes, leading to an increased fibrinolytic potential.
Materials And Methods:
This study examined the level of annexin II cell surface and mRNA expression in a range of acute myeloid leukaemia (AML) cell lines. The evidence that annexin II levels are higher in APL would lend support to the hypothesis that the bleeding disorder seen in APL is caused by hyperfibrinolysis.
Results:
Cell surface annexin II was found to be expressed at higher levels on NB4 (promyelocytic) cells than on either KG1a (early myeloid) or HL60 (myelocytic) cells. However, even higher levels were found on U937 and MM6 (histo-monocytic) and HEL (erythroid) cells (p<0.01). MM6 cells showed a threefold increase in annexin II mRNA compared to any of the other cell lines.
Conclusions:
These findings do not fully support the concept of the coagulopathy associated with APL being caused by hyperfibrinolysis alone. Further investigations are required to identify the significance of annexin II expression and regulation in leukaemia.
Insights
Annexin II is overexpressed in some leukemia cell lines, but not exclusively in acute promyelocytic leukemia (APL). This suggests hyperfibrinolysis alone may not explain APL coagulopathy.
Area of Science:
- Hematology
- Molecular Biology
- Oncology
Background:
- Acute promyelocytic leukemia (APL) is linked to bleeding disorders, potentially due to increased fibrinolysis.
- Annexin II, a coreceptor for tissue plasminogen activator and plasminogen, is hypothesized to be overexpressed in APL, enhancing fibrinolytic potential.
Purpose of the Study:
- To investigate annexin II cell surface and mRNA expression in various acute myeloid leukemia (AML) cell lines.
- To determine if elevated annexin II levels in APL support the hyperfibrinolysis hypothesis for bleeding diathesis.
Main Methods:
- Analysis of annexin II cell surface expression across different AML cell lines.
- Quantification of annexin II mRNA levels in these cell lines.
Main Results:
- Higher cell surface annexin II was observed in NB4 (APL) cells compared to KG1a and HL60 cells.
- U937, MM6, and HEL cells exhibited even higher annexin II cell surface expression.
- MM6 cells demonstrated a threefold increase in annexin II mRNA compared to other cell lines.
Conclusions:
- The findings do not fully support hyperfibrinolysis as the sole cause of coagulopathy in APL.
- Further research is needed to elucidate the role of annexin II expression and regulation in leukemia.
