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Heparin localization and fine structure regulate Burkitt's lymphoma growth
David Berry1, David M Lynn, Eric Berry
1Harvard Medical School, Boston, MA 02215, USA.
Biochemical and Biophysical Research Communications
|August 15, 2006
Summary
Heparan sulfate proteoglycans regulate Burkitt's lymphoma (BL) cell growth. External heparin inhibited BL growth, while internalized heparin promoted it, suggesting HSGAGs as a therapeutic target.
Area of Science:
- Oncology
- Biochemistry
- Molecular Biology
Background:
- Burkitt's lymphoma (BL) is a B-cell malignancy linked to Epstein-Barr virus (EBV).
- Heparan sulfate proteoglycans and heparan sulfate-like glycosaminoglycans (HSGAGs) are implicated in BL initiation, severity, and progression.
Purpose of the Study:
- To investigate the role of HSGAGs in regulating BL cell proliferation.
- To explore HSGAGs as potential therapeutic targets for BL.
Main Methods:
- Examined the effects of extracellular and internalized heparin on BL cell growth.
- Assessed the involvement of cell surface HSGAGs, PI3K, and Erk/Mek pathways.
- Utilized protamine sulfate and heparinases (specifically heparinase I) to inhibit proliferation.
Main Results:
- Extracellular heparin inhibited BL cell growth by over 30%.
- Heparin internalized with poly(beta-amino esters) promoted proliferation by up to 58%.
- Both heparin treatments' effects were dependent on cell surface HSGAGs, PI3K, and Erk/Mek signaling.
Conclusions:
- Cell surface HSGAGs play a significant role in regulating BL cell proliferation.
- Modulating HSGAGs, particularly with heparinase I, can inhibit BL proliferation.
- HSGAGs represent a promising therapeutic target for Burkitt's lymphoma intervention.
