Henriques, AndreiaMatos, PauloJordan, Peter2018-03-132018-03-132017-09Ann Oncol. 2017 Sept;28(Suppl 5):50-52. doi:10.1093/annonc/mdx361.036.0923-7534http://hdl.handle.net/10400.18/5393ESMO 2017 - 42nd European Society of Medical Oncology Congress 2017, 8-12 September 2017, Madrid, SpainBackground: Cancer cells require increased glucose supply to sustain proliferation. One mechanism involves increased expression of glucose transporter (GLUT) genes. But insulin has revealed that protein phosphorylation is another key mechanism in glucose uptake regulation: insulin binding to responsive cells triggers a signalling cascade with phosphorylation of TBC1D4, a negative regulator of endosomal GLUT trafficking, so that more transporters are inserted into the plasma membrane. Previous work from the host lab has identified the family of WNK protein kinases and shown that WNK1 can also phosphorylate TBC1D4 and promote GLUT translocation to the cell surface. Our objective is to understand the contribution of WNK1 to glucose uptake in colorectal cancer cells. Our objective is to understand the contribution of WNK1 to glucose uptake in colorectal cancer cells.engWNK Protein KinasesColorectal CancerTransporte de GlucoseVias de Transdução de Sinal e Patologias AssociadasCancro Coloretalconference object10.1093/annonc/mdx361.036