4.4 Article

The Potential Value of Microseminoprotein-β as a Prostate Cancer Biomarker and Therapeutic Target

期刊

PROSTATE
卷 70, 期 3, 页码 333-340

出版社

WILEY
DOI: 10.1002/pros.21059

关键词

MSMB; therapeutic; mutation

资金

  1. University of Cambridge, Cancer Research UK [C522/A8072, C5047/A3354]
  2. Institute of Cancer Research
  3. Hutchison Whampoa Limited
  4. National Institute for Health Research (NIHR)
  5. Bio-medical Research Centre at The Institute of Cancer Research
  6. Royal Marsden NHS Foundation Trust
  7. NCRI (ProMPT) Collaborative [60500966/75466]
  8. MRC [G0500966, G0501019] Funding Source: UKRI
  9. Medical Research Council [G0500966, G0501019] Funding Source: researchfish

向作者/读者索取更多资源

BACKGROUND. Recent genome-wide association studies have shown an association of a SNP two base pairs upstream of the 5' UTR of the microseminoprotein-beta (MSMB) gene with an increased risk of developing the prostate cancer, re-igniting interest in its protein product, MSMB. METHODS. As one of the most abundant prostatic proteins, MSMB can be reliably detected in tissue and serum. RESULTS. It has been consistently shown that MSMB expression is high in normal and benign prostate tissue and lowered or lost in prostate cancer suggesting that it might be a useful tissue biomarker for prostate cancer diagnosis and its levels in serum may be useful as a marker for prognosis. Members of the cysteine-rich secretory protein family and laminin receptors have been shown to bind MSMB at the cell surface and in serum thereby regulating apoptosis. Thus, in the benign prostate, MSMB regulates cell growth, but when MSMB is lost during tumourigenesis, cells are able to grow in a more uncontrolled manner. Both full length MSMB and a short peptide comprised of amino acids 31-45 have been tested for potential therapeutic benefit in mouse models and humans. CONCLUSIONS. MSMB has potential as a biomarker of prostate cancer development, progression and recurrence and potentially as a target for therapeutic intervention. Prostate 70: 333-340, 2010. (C) 2009 Wiley-Liss, Inc.

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