Semin Thromb Hemost 2007; 33(1): 080-086
DOI: 10.1055/s-2006-958466
Copyright © 2007 by Thieme Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA.

Prothrombotic Effects of Prostasomes Isolated from Prostatic Cancer Cell Lines and Seminal Plasma

Adil A. Babiker1 , Kristina Nilsson Ekdahl1 , 2 , Bo Nilsson1 , Gunnar Ronquist3
  • 1Department of Oncology, Radiology, and Clinical Immunology, Division of Clinical Immunology, Rudbeck Laboratory C5, Uppsala, Sweden
  • 2Department of Chemistry and Biomedical Sciences, University of Kalmar, Kalmar, Sweden
  • 3Department of Medical Sciences, Division of Clinical Chemistry, University Hospital, Uppsala, Sweden
Further Information

Publication History

Publication Date:
29 January 2007 (online)

ABSTRACT

Thromboembolism is well recognized as a major complication of cancer. Many tumor cells overexpress tissue factor (TF), which activates blood coagulation in cancer patients. Inflammatory cells expressing TF are also contributors to this activation. In prostate cancer, we believe that prostasomes may also be involved in the initiation of blood coagulation. Prostasomes are submicron secretory granules derived from the prostate gland. They are surrounded by membrane and their extracellular appearance and membrane architecture are complex. Seminal prostasomes are believed to be necessary for successful fertilization and act as protectors of the spermatozoa in the lower and upper female genital tract. Cells from prostate cancer and its metastases are able to produce and export prostasomes to the extracellular environment. These prostasomes may differ quantitatively rather than qualitatively from their normal counterparts with regard to protein composition and function. A majority of human prostate cancers have been found to overexpress TF, and we have demonstrated by various methods that prostasomes derived from prostate cancer cells express considerably higher levels of TF compared with prostasomes of nonmalignant cell origin. The mechanism related to thromboembolic disease generated by prostasomes in prostatic cancer patients may be the early release of prostasomes from prostate cancer cells into the blood circulation, where they will evoke their blood-clotting effects.

REFERENCES

Professor Gunnar Ronquist

Department of Medical Sciences, Clinical Chemistry

University Hospital SE-751 85 Uppsala, Sweden

Email: [email protected]