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Metabolic profiling reveals PAFAH1B3 as a critical driver of breast cancer pathogenicity.


ABSTRACT: Many studies have identified metabolic pathways that underlie cellular transformation, but the metabolic drivers of cancer progression remain less well understood. The Hippo transducer pathway has been shown to confer malignant traits on breast cancer cells. In this study, we used metabolic mapping platforms to identify biochemical drivers of cellular transformation and malignant progression driven through RAS and the Hippo pathway in breast cancer and identified platelet-activating factor acetylhydrolase 1B3 (PAFAH1B3) as a key metabolic driver of breast cancer pathogenicity that is upregulated in primary human breast tumors and correlated with poor prognosis. Metabolomic profiling suggests that PAFAH1B3 inactivation attenuates cancer pathogenicity through enhancing tumor-suppressing signaling lipids. Our studies provide a map of altered metabolism that underlies breast cancer progression and put forth PAFAH1B3 as a critical metabolic node in breast cancer.

SUBMITTER: Mulvihill MM 

PROVIDER: S-EPMC4119799 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature

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Metabolic profiling reveals PAFAH1B3 as a critical driver of breast cancer pathogenicity.

Mulvihill Melinda M MM   Benjamin Daniel I DI   Ji Xiaodan X   Le Scolan Erwan E   Louie Sharon M SM   Shieh Alice A   Green McKenna M   Narasimhalu Tara T   Morris Patrick J PJ   Luo Kunxin K   Nomura Daniel K DK  

Chemistry & biology 20140619 7


Many studies have identified metabolic pathways that underlie cellular transformation, but the metabolic drivers of cancer progression remain less well understood. The Hippo transducer pathway has been shown to confer malignant traits on breast cancer cells. In this study, we used metabolic mapping platforms to identify biochemical drivers of cellular transformation and malignant progression driven through RAS and the Hippo pathway in breast cancer and identified platelet-activating factor acety  ...[more]

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