Andreia F.A. Henriques (a,b), Paulo Matos (a,b), Ana Sofia Carvalho ()c, Mikel Azkargorta (d), Felix Elortza (d), Rune Matthiesen (c), Peter Jordan (a,b)
a Department of Human Genetics, National Health Institute ‘Dr. Ricardo Jorge’, Lisbon, Portugal
b BioISI - Biosystems & Integrative Sciences Institute, Faculty of Sciences, University of Lisbon, Lisbon, Portugal
Neste trabalho foi estudada a regulação da entrada de glucose para o interior da célula, um mecanismo chave para o metabolismo celular no corpo, mas também para o sustento da alta taxa proliferativa das células cancerígenas. Além dos níveis de expressão dos transportadores GLUT, que são os principais responsáveis pela entrada de glucose, existe um segundo mecanismo de regulação: a sua inserção na membrana plasmática (MP) a partir de vesículas intracelulares, sob controlo de vias de sinalização.
Tumour initiation results from a mutation acquired, for example, in a cell proliferation-regulating oncogene, for example the MAP kinase BRAF in melanoma, thyroid, ovarian and colorectal cancer. As a protective response to this initial proliferative stimulus, tissues induce a growth-arrest program termed oncogene-induced senescence (OIS). It remains largely unknown by which mechanisms the initiated cells eventually escape from the dormant OIS state.
Tumour initiation results from a mutation acquired, for example, in a cell proliferation-regulating oncogene, for example the MAP kinase BRAF in melanoma, thyroid, ovarian and colorectal cancer. As a protective response to this initial proliferative stimulus, tissues induce a growth-arrest program termed oncogene-induced senescence (OIS). It remains largely unknown by which mechanisms the initiated cells eventually escape from the dormant OIS state.
