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Horsch, M. ; Recktenwald, C.V.* ; Schädler, S. ; Hrabě de Angelis, M. ; Seliger, B.* ; Beckers, J.

Overexpressed vs mutated Kras in murine fibroblasts: A molecular phenotyping study.

Br. J. Cancer 100, 656-662 (2009)
Verlagsversion DOI PMC
Free by publisher
Creative Commons Lizenzvertrag
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Ras acts in signalling pathways regulating the activity of multiple cellular functions including cell proliferation, differentiation, and apoptosis. Amino-acid exchanges at position 12, 13, or 61 of the Kras gene convert the proto-oncogene into an activated oncogene. Until now, a direct comparison of genome-wide expression profiling studies of Kras overexpression and different Kras mutant forms in a single assay system has not been carried out. In our study, we focused on the direct comparison of global gene expression effects caused by mutations in codon 12 or 13 of the Kras gene and Kras overexpression in murine fibroblasts. We determined Kras cellular mRNA, Ras protein and activated Ras protein levels. Further, we compared our data to the proteome analysis of the same transfected cell lines. Both overexpression and mutations of Kras lead to common altered gene expression patterns. Only two genes, Lox and Col1a1, were reversely regulated in the Kras transfectants. They may contribute to the higher aggressiveness of the Kras codon 12 mutation in tumour progression. The functional annotation of differentially expressed genes revealed a high frequency of proteins involved in tumour growth and angiogenesis. These data further support the important role of these genes in tumour-associated angiogenesis.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Kras mutation; Kras overexpression; murine fibroblast cell lines; gene-expression profiling; lysyl-oxidase; gene-expression; breast-cancer; ki-ras; copper-binding; human-colon; transformation; mutations; tumors; activation
ISSN (print) / ISBN 0007-0920
e-ISSN 1532-1827
Zeitschrift British Journal of Cancer BJC
Quellenangaben Band: 100, Heft: 4, Seiten: 656-662 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Experimental Genetics (IEG)