Journal
MOLECULAR CANCER
Volume 11, Issue -, Pages -Publisher
BMC
DOI: 10.1186/1476-4598-11-15
Keywords
c-Myb; Metastasis; Breast cancer; Matrix metalloproteinase; Cathepsin D; Extracellular matrix
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Funding
- Czech Science Foundation [301/09/1115, 204/08/H054]
- Ministry of Education, Youth, and Sports of the Czech Republic [MSM0021622415]
- International Clinical Research Center [CZ.1.05/1.1.00/02.0123]
- Grant Agency of Academy of Sciences [IAA501630901]
- Ministry of Health of the Czech Republic [IGA MZD9600-4/2008]
- Masaryk University [MUNI/C/0968/2011]
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Background: The c-Myb transcription factor is essential for the maintenance of stem-progenitor cells in bone marrow, colon epithelia, and neurogenic niches. c-Myb malfunction contributes to several types of malignancies including breast cancer. However, the function of c-Myb in the metastatic spread of breast tumors remains unexplored. In this study, we report a novel role of c-Myb in the control of specific proteases that regulate the matrix-dependent invasion of breast cancer cells. Results: Ectopically expressed c-Myb enhanced migration and ability of human MDA-MB-231 and mouse 4T1 mammary cancer cells to invade Matrigel but not the collagen I matrix in vitro. c-Myb strongly increased the expression/activity of cathepsin D and matrix metalloproteinase (MMP) 9 and significantly downregulated MMP1. The gene coding for cathepsin D was suggested as the c-Myb-responsive gene and downstream effector of the migration-promoting function of c-Myb. Finally, we demonstrated that c-Myb delayed the growth of mammary tumors in BALB/c mice and affected the metastatic potential of breast cancer cells in an organ-specific manner. Conclusions: This study identified c-Myb as a matrix-dependent regulator of invasive behavior of breast cancer cells.
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