2012
Knopfová, Lucia; Beneš, Petr; Pekarčíková, Lucie; Hermanová, Markéta; Masařík, Michal; Pernicová, Zuzana; Souček, Karel; Smarda, Jan
c-Myb regulates matrix metalloproteinases 1/9, and cathepsin D: implications for matrix-dependent breast cancer cell invasion and metastasis. Journal Article
In: Molecular cancer, vol. 11, pp. 15, 2012, ISSN: 1476-4598, (Place: England).
Abstract | Links | BibTeX | Tags: Animals, Breast Neoplasms/genetics/*metabolism, Cathepsin D/genetics/*metabolism, Cell Line, Cell Movement/genetics/physiology, Electrophoresis, Female, Humans, Immunoblotting, Inbred BALB C, Matrix Metalloproteinase 1/genetics/*metabolism, Matrix Metalloproteinase 9/genetics/*metabolism, Mice, Neoplasm Metastasis/genetics/physiopathology, Polyacrylamide Gel, Proto-Oncogene Proteins c-myb/genetics/*metabolism, Real-Time Polymerase Chain Reaction, RNA, Small Interfering, Tumor
@article{knopfova_c-myb_2012,
title = {c-Myb regulates matrix metalloproteinases 1/9, and cathepsin D: implications for matrix-dependent breast cancer cell invasion and metastasis.},
author = {Lucia Knopfová and Petr Beneš and Lucie Pekarčíková and Markéta Hermanová and Michal Masařík and Zuzana Pernicová and Karel Souček and Jan Smarda},
doi = {10.1186/1476-4598-11-15},
issn = {1476-4598},
year = {2012},
date = {2012-03-01},
journal = {Molecular cancer},
volume = {11},
pages = {15},
abstract = {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.},
note = {Place: England},
keywords = {Animals, Breast Neoplasms/genetics/*metabolism, Cathepsin D/genetics/*metabolism, Cell Line, Cell Movement/genetics/physiology, Electrophoresis, Female, Humans, Immunoblotting, Inbred BALB C, Matrix Metalloproteinase 1/genetics/*metabolism, Matrix Metalloproteinase 9/genetics/*metabolism, Mice, Neoplasm Metastasis/genetics/physiopathology, Polyacrylamide Gel, Proto-Oncogene Proteins c-myb/genetics/*metabolism, Real-Time Polymerase Chain Reaction, RNA, Small Interfering, Tumor},
pubstate = {published},
tppubtype = {article}
}
2011
Benes, Petr; Knopfova, Lucia; Trcka, Filip; Nemajerova, Alice; Pinheiro, Diana; Soucek, Karel; Fojta, Miroslav; Smarda, Jan
Inhibition of topoisomerase IIα: novel function of wedelolactone. Journal Article
In: Cancer letters, vol. 303, no. 1, pp. 29–38, 2011, ISSN: 1872-7980 0304-3835, (Place: Ireland).
Abstract | Links | BibTeX | Tags: Antigens, Antineoplastic Agents/pharmacology, Apoptosis/drug effects, Breast Neoplasms/*drug therapy/enzymology/pathology, Cell Cycle/drug effects, Cell Growth Processes/drug effects, Cell Line, Cell Survival/drug effects, Coumarins/*pharmacology, DNA Damage, DNA Topoisomerases, DNA-Binding Proteins/*antagonists & inhibitors/metabolism, Enzyme-Linked Immunosorbent Assay, Female, Humans, Immunoblotting, Neoplasm/metabolism, Signal Transduction, Topoisomerase Inhibitors/*pharmacology, Tumor, Type II/metabolism
@article{benes_inhibition_2011,
title = {Inhibition of topoisomerase IIα: novel function of wedelolactone.},
author = {Petr Benes and Lucia Knopfova and Filip Trcka and Alice Nemajerova and Diana Pinheiro and Karel Soucek and Miroslav Fojta and Jan Smarda},
doi = {10.1016/j.canlet.2011.01.002},
issn = {1872-7980 0304-3835},
year = {2011},
date = {2011-04-01},
journal = {Cancer letters},
volume = {303},
number = {1},
pages = {29–38},
abstract = {The naturally occurring coumestan wedelolactone has been previously shown to reduce growth of various cancer cells. So far, the growth-suppressing effect of wedelolactone has been attributed to the inhibition of the NFκB transcription factor and/or androgen receptors. We found that wedelolactone suppressed growth and induced apoptosis of androgen receptor-negative MDA-MB-231 breast cancer cells at concentrations that did not inhibit the NFκB activity. The cells responded to wedelolactone by the S and G2/M phase cell cycle arrest and induction of the DNA damage signaling. Wedelolactone interacted with dsDNA and inhibited the activity of DNA topoisomerase IIα. We conclude that wedelolactone can act as growth suppressor independently of NFκB and androgen receptors.},
note = {Place: Ireland},
keywords = {Antigens, Antineoplastic Agents/pharmacology, Apoptosis/drug effects, Breast Neoplasms/*drug therapy/enzymology/pathology, Cell Cycle/drug effects, Cell Growth Processes/drug effects, Cell Line, Cell Survival/drug effects, Coumarins/*pharmacology, DNA Damage, DNA Topoisomerases, DNA-Binding Proteins/*antagonists & inhibitors/metabolism, Enzyme-Linked Immunosorbent Assay, Female, Humans, Immunoblotting, Neoplasm/metabolism, Signal Transduction, Topoisomerase Inhibitors/*pharmacology, Tumor, Type II/metabolism},
pubstate = {published},
tppubtype = {article}
}