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Compensatory metabolic networks in pancreatic cancers upon perturbation of glutamine metabolism.

Abstract：

:Pancreatic ductal adenocarcinoma is a notoriously difficult-to-treat cancer and patients are in need of novel therapies. We have shown previously that these tumours have altered metabolic requirements, making them highly reliant on a number of adaptations including a non-canonical glutamine (Gln) metabolic pathway and that inhibition of downstream components of Gln metabolism leads to a decrease in tumour growth. Here we test whether recently developed inhibitors of glutaminase (GLS), which mediates an early step in Gln metabolism, represent a viable therapeutic strategy. We show that despite marked early effects on in vitro proliferation caused by GLS inhibition, pancreatic cancer cells have adaptive metabolic networks that sustain proliferation in vitro and in vivo. We use an integrated metabolomic and proteomic platform to understand this adaptive response and thereby design rational combinatorial approaches. We demonstrate that pancreatic cancer metabolism is adaptive and that targeting Gln metabolism in combination with these adaptive responses may yield clinical benefits for patients.

journal_name

Nat Commun

journal_title

Nature communications

authors

Biancur DE,Paulo JA,Małachowska B,Quiles Del Rey M,Sousa CM,Wang X,Sohn ASW,Chu GC,Gygi SP,Harper JW,Fendler W,Mancias JD,Kimmelman AC

doi

10.1038/ncomms15965

subject

Has Abstract

pub_date

2017-07-03 00:00:00

pages

15965

issn

2041-1723

pii

ncomms15965

journal_volume

8

pub_type

杂志文章

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