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001-es BibID:	BIBFORM004861
035-os BibID:	(scopus)14644392200 (wos)000227768400023
Első szerző:	Diermeier, Simone
Cím:	Epidermal growth factor receptor coexpression modulates susceptibility to Herceptin in HER2/neu overexpressing breast cancer cells via specific erbB-receptor interaction and activation / Diermeier, S., Horvath, G., Knuechel-Clarke, R., Hofstaedter, F., Szollosi, J., Brockhoff, G.
Dátum:	2005
ISSN:	0014-4827
Megjegyzések:	Growth factors and Herceptin specifically and differentially modulate cell proliferation of tumor cells. However, the mechanism of action on erbB-receptor level is incompletely understood. We evaluated Herceptin's capacity to modulate erbB-receptor activation and interaction on the cell surface level and thereby potentially impair cell proliferation of HER2/neu (c-erbB2) overexpressing breast cancer cells, both in the presence and absence of relevant growth factors. METHODS: BT474 and SK-BR-3 breast cancer cell lines were treated with Epidermal Growth Factor (EGF), Heregulin, and with Herceptin in different combinations. Kinetics of cell proliferation were evaluated flow cytometrically based on BrdU-labeling. Fluorescence Resonance Energy Transfer, ELISAs and phosphorylation site specific Western Blotting was performed to investigate erbB-receptor interaction and activation. RESULTS: EGF induced EGFR/EGFR and EGFR/c-erbB2 interactions correlate with stimulation of cell proliferation in BT474 cells. Both homo- and heterodimerization are considerably less pronounced in SK-BR-3 cells and heterointeraction is additionally reduced by EGF treatment, causing inhibition of cell proliferation. Heregulin stimulates cell proliferation extensively in both cell lines. Herceptin drives BT474 cells more efficiently into quiescence than it does with SK-BR-3 cells and thereby blocks cell cycle progress. In SK-BR-3 Herceptin treatment causes c-erbB2 phosphorylation of Y877 and Y1248, EGF induces Y877 and Y1112 phosphorylation. The Y1112 phosphorylation site, activated by EGF in SK-BR-3 cell, is bypassed in BT474. In addition the inhibitory capacity of Herceptin on BT474 and SK-BR-3 cell proliferation depends on the presence and absence of growth factors to a various extent. CONCLUSION: The growth inhibitory effect of Herceptin on c-erbB2 overexpressing breast cancer cells is considerably modulated by EGFR coexpression and consequently EGFR/c-erbB2 homo- and heterointeractions, as well as the presence or absence of growth factors. C-erbB2 overexpression alone is insufficient to predict the impact of growth factors and antibodies on cell proliferation. The optimization and specification of therapeutic approaches based on erbB-receptor targeting requires to account for EGFR coexpression as well as the potential presence of erbB-receptor relevant growth factors.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Antibodies Antibodies,Monoclonal Antineoplastic Agents Breast Neoplasms Carcinoma Cell Cycle Cell Cycle Proteins Cell Line Cell Line, Tumor Cell Proliferation Cells drug effects Drug Resistance,Neoplasm Drug Synergism drug therapy Energy Transfer Epidermal Growth Factor Female Fluorescence Fluorescence Resonance Energy Transfer genetics Growth Inhibitors Humans Kinetics metabolism methods Neuregulin-1 pathology pharmacology Phosphorylation physiology Proteins Receptor, Epidermal Growth Factor Receptor, erbB-2 Receptors, Cell Surface Research Support therapeutic use
Megjelenés:	Experimental Cell Research. - 304 : 2 (2005), p. 604-619. -
További szerzők:	Horváth Gábor (1974-) (biofizikus) Knuechel-Clarke, Ruth Hofstaedter, Ferdinand Szöllősi János (1953-) (biofizikus) Brockhoff, Gero
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001-es BibID:	BIBFORM003553
Első szerző:	Kakuk Annamária (molekuláris biológus)
Cím:	Nuclear and nucleolar localization signals and their targeting function in phosphatidylinositol 4-kinase PI4K230 / Kakuk A., Friedlander E., Vereb Gy. Jr., Lisboa, D., Bagossi P., Tóth G., Gergely P., Vereb Gy.
Dátum:	2008
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban phosphatidylinositol 4-kinase PI4K230 nuclear localization signal NLS nucleolar targeting NTS importins permeabilized HeLa cells import assay
Megjelenés:	Experimental Cell Research. - 314 : 13 (2008), p. 2376-2388. -
További szerzők:	Friedländer Elza (1980-) (biofizikus) Vereb György (1965-) (biofizikus, orvos) Lisboa, Duarte (1982-) (biotechnológus) Bagossi Péter (1966-2011) (biokémikus, vegyész) Tóth Gábor Gergely Pál (1947-) (biokémikus) Vereb György (1938-) (biokémikus, sejtbiológus)
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001-es BibID:	BIBFORM004735
Első szerző:	Nagy Péter (biofizikus)
Cím:	Small interfering RNAs suppress the expression of endogenous and GFP-fused epidermal growth factor receptor (erbB1) and induce apoptosis in erbB1-overexpressing cells / Nagy, P., Arndt-Jovin, D. J., Jovin, T. M.
Dátum:	2003
ISSN:	014-4827 (Print)
Megjegyzések:	Deregulated and excessive expression of epidermal growth factor receptor (EGFR or erbB1), a transmembrane receptor tyrosine kinase specific for the epidermal growth factor (EGF), is a feature and/or cause of a wide range of human cancers, and thus inhibition of its expression is potentially therapeutic. In RNA interference (RNAi), duplexes of 21-nucleotide RNAs (small interfering RNA, siRNA) corresponding to mRNA sequences of particular genes are used to efficiently inhibit the expression of the target proteins in mammalian cells. Here we show that by using RNAi the expression of endogenous erbB1 can be specifically and extensively (90%) suppressed in A431 human epidermoid carcinoma cells. As a consequence, EGF-induced tyrosine phosphorylation was inhibited and cell proliferation was reduced due to induction of apoptosis. We established an inverse correlation between the level of expressed erbB1 and EGF sensitivity on a cell-by-cell basis using flow cytometry. A431 cells expressing endogenous erbB1 were transfected with erbB1 fused C-terminally to enhanced green fluorescent protein (EGFP). Selective inhibition of the expression of the fusion protein was achieved with an siRNA specific for the EGFP mRNA, whereas the erbB1-specific siRNAs inhibited the expression of both molecules. siRNA-mediated inhibition of erbB1 and other erbB tyrosine kinases may constitute a useful therapeutic approach in the treatment of human cancer.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Animals Apoptosis Carcinoma Cell Cycle Cell Line Cell Proliferation Cells chemistry Epidermal Growth Factor Flow Cytometry genetics Green Fluorescent Proteins Human Humans Indicators and Reagents Luminescent Proteins metabolism Microscopy,Fluorescence Phosphorylation physiology Proteins Receptor, Epidermal Growth Factor Recombinant Fusion Proteins Research RNA,Small Interfering Support Tyrosine
Megjelenés:	Experimental Cell Research. - 285 : 1 (2003), p. 39-49. -
További szerzők:	Arndt-Jovin, Donna J. Jovin, Thomas M.
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