KNOPFOVÁ, Lucia, Petr BENEŠ, Lucie PEKARČÍKOVÁ, Markéta HERMANOVÁ, Michal MASAŘÍK and Jan ŠMARDA. Regulation of cathepsin D and MMP1/9 by c-Myb is a novel mechanism of the matrix-specific breast cancer cell invasion. In EMBO. Cellular Signaling and Molecular Medicine. Cavtat, Dubrovnik: EMBO, 2012, p. 131.
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Basic information
Original name Regulation of cathepsin D and MMP1/9 by c-Myb is a novel mechanism of the matrix-specific breast cancer cell invasion
Name in Czech c-Myb reguluje MMP1/9 a cathepsin D - nový mechanismus matrix-dependentní invaze prsních nádorů
Authors KNOPFOVÁ, Lucia, Petr BENEŠ, Lucie PEKARČÍKOVÁ, Markéta HERMANOVÁ, Michal MASAŘÍK and Jan ŠMARDA.
Edition Cavtat, Dubrovnik, Cellular Signaling and Molecular Medicine, p. 131-131, 2012.
Publisher EMBO
Other information
Original language English
Type of outcome Proceedings paper
Field of Study Genetics and molecular biology
Confidentiality degree is not subject to a state or trade secret
Organization unit Faculty of Science
Keywords in English myb breast carcinoma metastasis organotropism
Tags myb breast carcinoma metastasis organotropism
Tags International impact
Changed by Changed by: prof. RNDr. Jan Šmarda, CSc., učo 1223. Changed: 14/8/2012 14:42.
Abstract
There are conflicting results concerning the c-Myb function in breast cancer. Both oncogenic and tumor-suppressing effects of c-Myb in breast cancer have been recently described. The aim of this study is to elucidate a specific role of c-Myb in control of breast cancer cell invasion. We report that ectopically expressed c-Myb enhances migration of human MDA-MB-231 and mouse 4T1 mammary cancer cells and their ability to invade Matrigel but not the collagen I matrix in vitro. Invasive behavior of breast cancer cells in vivo was determined in a syngeneic mouse mammary tumor model using 4T1 cells. c-myb overexpression in 4T1 cells injected into the mammary fat pads delayed the growth of mammary tumors in BALB/c mice and affected the metastatic potential of breast cancer cells in an organ-specific manner. c-Myb strongly increased the expression/activity of cathepsin D and matrix metalloproteinase (MMP) 9 (92-kDa gelatinase) and significantly downregulated MMP1 (interstitial collagenase). Differential expression of these specific proteases induced by c-Myb was suggested as a mechanism of matrix-specific cell invasion. This study identified c-Myb as a matrix-dependent modifier of invasive breast tumor cell functions. These findings provide new clues for understanding of the oncogenic/tumor-suppressing functions of c-Myb.
Links
GA301/09/1115, research and development projectName: Úloha proteinů c-Myb a Cox-2 při tvorbě střevních nádorů
Investor: Czech Science Foundation, The role of c-Myb and Cox-2 proteins in colon carcinogenesis
GD204/08/H054, research and development projectName: Molekulární mechanismy proliferace a diferenciace buněk
Investor: Czech Science Foundation, Molecular mechanisms of the cell proliferation and differentiation
MSM0021622415, plan (intention)Name: Molekulární podstata buněčných a tkáňových regulací
Investor: Ministry of Education, Youth and Sports of the CR, Molecular basis of cell and tissue regulations
MUNI/C/0968/2010, interní kód MUName: Úloha proteinu c-Myb v regulaci migrace, invazivity a apoptózy buněk střevního karcinomu (Acronym: c-Myb a invazivita CT26)
Investor: Masaryk University, Rector's Program
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