Utilize este identificador para referenciar este registo: http://hdl.handle.net/10400.18/3403
Título: B-Raf-induced senescence in colorectal cells is antagonized by expression of tumour-related Rac1b
Autor: Henriques, Andreia
Barros, Patrícia
Moyer, Mary
Matos, Paulo
Jordan, Peter
Palavras-chave: Vias de Transdução de Sinal e Patologias Associadas
Colorectal Cancer
BRaf
Rac1b
Senescence
Data: Ago-2015
Resumo: Mutations in the BRAF oncogene have been identified as a tumour-initiating genetic event in mainly melanoma, thyroid and colon cancer, resulting in an initial proliferative stimulus that is followed by a growth arrest period known as oncogene-induced senescence (OIS). It remains unknown what triggers subsequent escape from OIS to allow further tumour progression. A previous analysis revealed that around 80% of colorectal tumours carrying a mutation in BRAF also overexpress splice variant Rac1b. We used normal NCM460 colonocytes as a model to express oncogenic B-Raf-V600E in the presence or absence of co-transfected Rac1b and analysed the effect on expression the senescence marker β-galactosidase and of the cell-cycle inhibitors p14, p15 and p21. We provide evidence that co-expression of splice variant Rac1b counteracts B-Raf-induced senescence. When oncogenic B-Raf-V600E was expressed we observed the induction of the senescence marker β-galactosidase and of the cell-cycle inhibitors p14, p15 and p21. Upon co-expression of splice variant Rac1b, the B-Raf-induced senescence was relieved and expression of the cell-cycle inhibitor proteins downregulated. Our data indicate the selection for increased Rac1b expression as one potential mechanism by which colorectal tumour cells can escape from B-Raf-induced OIS.
Peer review: no
URI: http://hdl.handle.net/10400.18/3403
Aparece nas colecções:DGH - Posters/abstracts em congressos internacionais

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