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@article{Newton:2020:10.1038/s41467-020-18502-9,
author = {Newton, H and Wang, Y-F and Camplese, L and Mokochinski, JB and Kramer, HB and Brown, AEX and Fets, L and Hirabayashi, S},
doi = {10.1038/s41467-020-18502-9},
journal = {Nature Communications},
title = {Systemic muscle wasting and coordinated tumour response drive tumourigenesis},
url = {http://dx.doi.org/10.1038/s41467-020-18502-9},
volume = {11},
year = {2020}
}

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TY  - JOUR
AB  - Cancer cells demand excess nutrients to support their proliferation, but how tumours exploit extracellular amino acids during systemic metabolic perturbations remain incompletely understood. Here, we use a Drosophila model of high-sugar diet (HSD)-enhanced tumourigenesis to uncover a systemic host-tumour metabolic circuit that supports tumour growth. We demonstrate coordinate induction of systemic muscle wasting with tumour-autonomous Yorkie-mediated SLC36-family amino acid transporter expression as a proline-scavenging programme to drive tumourigenesis. We identify Indole-3-propionic acid as an optimal amino acid derivative to rationally target the proline-dependency of tumour growth. Insights from this whole-animal Drosophila model provide a powerful approach towards the identification and therapeutic exploitation of the amino acid vulnerabilities of tumourigenesis in the context of a perturbed systemic metabolic network.
AU  - Newton,H
AU  - Wang,Y-F
AU  - Camplese,L
AU  - Mokochinski,JB
AU  - Kramer,HB
AU  - Brown,AEX
AU  - Fets,L
AU  - Hirabayashi,S
DO  - 10.1038/s41467-020-18502-9
PY  - 2020///
SN  - 2041-1723
TI  - Systemic muscle wasting and coordinated tumour response drive tumourigenesis
T2  - Nature Communications
UR  - http://dx.doi.org/10.1038/s41467-020-18502-9
UR  - https://www.ncbi.nlm.nih.gov/pubmed/32938923
UR  - http://hdl.handle.net/10044/1/82889
VL  - 11
ER  -

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