Explore the words cloud of the NuSiCC project. It provides you a very rough idea of what is the project "NuSiCC" about.
The following table provides information about the project.
UNIVERSITY OF GLASGOW
|Coordinator Country||United Kingdom [UK]|
|Total cost||183˙454 €|
|EC max contribution||183˙454 € (100%)|
1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
|Duration (year-month-day)||from 2016-06-01 to 2018-05-31|
Take a look of project's partnership.
|1||UNIVERSITY OF GLASGOW||UK (GLASGOW)||coordinator||183˙454.00|
Colorectal cancer (CRC) kills up to 170,000 Europeans annually. Although survival rates have improved gradually, new treatment strategies are certainly needed. Hyper-activation of WNT/Beta-catenin signalling occurs in up 93% of CRC cases and MYC appears to be an obligate effector of Beta-Catenin in the gut, making MYC an attractive target for therapeutic intervention. MYC, however, is difficult to target directly, owing to its lack of enzymatic activity or obviously druggable structural features. An alternative strategy is to target the biological consequences of MYC deregulation. The Murphy lab recently showed that MYC overexpressing tumour cells in culture exhibit an ectopic dependency on a little-known kinase called ARK5/NUAK1: whereas cells lacking MYC overexpression are able to withstand NUAK1 depletion or inhibition, cells with overexpressed MYC are unable to maintain energetic homeostasis in the absence of NUAK1, deplete their ATP levels, and consequently lose viability. We have therefor taken a genetic approach to examine the requirement for NUAK1 during tumour development in a genetically engineered mouse model of sporadic Beta-Catenin-driven CRC. Our preliminary results show that NUAK1 is required for CR tumour initiation and, more importantly, that NUAK1 depletion shrinks pre-existing tumours, suggesting that NUAK1 is an excellent candidate target for treatment of CRC. Based on these exciting preliminary data, I now propose to thoroughly evaluate NUAK1 as a target for therapy in CRC and to use a combination of proteomic, phosphor-proteomic and metabolomics analysis to determine the mechanism by which NUAK1 suppression erodes tumour cell viability.
|year||authors and title||journal||last update|
BjÃ¶rn Kruspig, Tiziana Monteverde, Sarah Neidler, Andreas Hock, Emma Kerr, Colin Nixon, William Clark, Ann Hedley, Sarah Laing, Seth B. Coffelt, John Le Quesne, Craig Dick, Karen Vousden, Carla P. Martins, Daniel J. Murphy
The ERBB network facilitates KRAS-driven lung tumorigenesis
published pages: eaao2565, ISSN: 1946-6234, DOI: 10.1126/scitranslmed.aao2565
|Science Translational Medicine 10/446||2019-06-13|
Jennifer Port, Nathiya Muthalagu, Meera Raja, Fatih Ceteci, Tiziana Monteverde, BjÃ¶rn Kruspig, Ann Hedley, Gabriela Kalna, Sergio Lilla, Lisa Neilson, Martina Brucoli, Katarina Gyuraszova, Jacqueline Tait-Mulder, Mokdad Mezna, Silvija Svambaryte, Amy Bryson, David Sumpton, Allan McVie, Colin Nixon, Martin Drysdale, Hiroyasu Esumi, Graeme I. Murray, Owen J. Sansom, Sara R. Zanivan, Daniel J. Murphy
Colorectal Tumors Require NUAK1 for Protection from Oxidative Stress
published pages: 632-647, ISSN: 2159-8274, DOI: 10.1158/2159-8290.CD-17-0533
|Cancer Discovery 8/5||2019-06-13|
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The information about "NUSICC" are provided by the European Opendata Portal: CORDIS opendata.
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