British Journal of Medicine and Medical Research, ISSN: 2231-0614,Vol.: 2, Issue.: 3 (July-September)
YKL-40: a Potential Biomarker and Therapeutic Target for Breast Cancer Diagnosis and Therapy
Rong Shao1,2,3* 1Molecular and Cellular Biology Program, Morrill Science Center, University of Massachusetts, Amherst, MA 01003, U.S.A.
2Pioneer Valley Life Sciences Institute, 3601 Main Street, Springfield, MA 01199, U.S.A.
3Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA 01003, U.S.A.
1Molecular and Cellular Biology Program, Morrill Science Center, University of Massachusetts, Amherst, MA 01003, U.S.A.
Over the past two decades, emerging data have found that YKL-40, a secreted glycoprotein, is elevated in a broad spectrum of human diseases including cancers, liver injury, asthma, diabetes, inflammatory diseases, and cardiac disorders. In breast cancer, increased serum levels of YKL-40 are correlated with cancer metastasis and short survival, suggesting that serum levels of YKL-40 serve as a cancer biomarker. YKL-40 has the ability to stimulate vascular endothelial cell activation and suppress mammary epithelial cell differentiation, the pathophysiological events associated with tumor angiogenesis and poor differentiation. Neutralization of YKL-40 via an anti-YKL-40 monoclonal antibody in animal trials demonstrates the ability of YKL-40 blockade to impede tumor angiogenesis and tumor growth, thus holding therapeutic promise for cancer therapy. Apart from these findings, substantial efforts are urgently required to decipher the key molecular mechanisms that mediate cancer metastasis and malignancy, which is expected to significantly offer translational value for breast cancer diagnosis, prognosis and therapy. This review discusses the current status of research on YKL-40’s expression, biophysiological and pathological activities and functional inhibition, which is instrumental for future clinical practice.
YKL-40; cancer biomarker; therapeutic target; breast cancer.
DOI : 10.9734/BJMMR/2012/1282Review History Comments