Relationships of lipocalin 2 with breast tumorigenesis and metastasis

• Published in: Journal of cellular physiology 2011-02, Vol.226 (2), p.309-314
• Main Authors: Leng, Xiaohong, Wu, Yun, Arlinghaus, Ralph B.
• Format: Article
• Language: English
• Subjects: Acute-Phase Proteins - genetics; Acute-Phase Proteins - metabolism; Animals; Biomarkers, Tumor - genetics; Biomarkers, Tumor - metabolism; Breast Neoplasms - genetics; Breast Neoplasms - metabolism; Breast Neoplasms - pathology; Epithelial-Mesenchymal Transition; Female; Humans; Iron - metabolism; Leukemia - metabolism; Leukemia - pathology; Lipocalin-2; Lipocalins - genetics; Lipocalins - metabolism; Matrix Metalloproteinase 9 - metabolism; Neoplasm Metastasis; Proto-Oncogene Proteins - genetics; Proto-Oncogene Proteins - metabolism
• ISSN: 0021-9541; 1097-4652
• DOI: 10.1002/jcp.22403

Breast cancer is one of the most common cancers in women worldwide and accounts for one‐sixth of cancer deaths in the United States. Breast cancer consists of a heterogeneous group of tumours classified into five types, in which the HER2/neu positive and the basal type (most are ER and HER2 negative) have the worst clinical prognosis. In recent years, prognostic/predictive markers such as ER/PR or HER2/neu have been widely used in the selection of the optimal breast cancer treatments for individual patients, which have been proven to be very effective in disease control. These results suggest that further examination of the molecular mechanisms underlying the breast tumorigenesis and identification of the potential biomarkers in different types of breast cancers will greatly benefit clinical diagnosis and facilitate the design of more effective personalized therapies to increase patient survival. This review aims to summarize recent research findings on lipocalin 2 (LCN2), a newly identified biomarker and a potential therapeutic target for breast cancer, and the possible mechanisms underlying its role in tumorigenesis and metastasis. J. Cell. Physiol. 226: 309–314, 2011. © 2010 Wiley‐Liss, Inc.