scholarly journals Up-regulation of Acetyl-CoA Carboxylase α and Fatty Acid Synthase by Human Epidermal Growth Factor Receptor 2 at the Translational Level in Breast Cancer Cells

2007 ◽  
Vol 282 (36) ◽  
pp. 26122-26131 ◽  
Author(s):  
Sarah Yoon ◽  
Min-Young Lee ◽  
Sahng Wook Park ◽  
Jong-Seok Moon ◽  
Yoo-Kyung Koh ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Fatty Acid ◽  
Growth Factor ◽  
Breast Cancer Cells ◽  
Fatty Acid Synthase ◽  
Growth Factor Receptor ◽  
Acetyl Coa Carboxylase ◽  
Epidermal Growth ◽  
Translational Level

TAMI-05. FATTY ACID SYNTHESIS IS REQUIRED FOR HER2+ BREAST CANCER BRAIN METASTASIS

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi199-vi199
Author(s):  
Gino Ferraro ◽  
Ahmed Ali ◽  
Alba Luengo ◽  
Amy Deik ◽  
Keene Abbott ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Fatty Acid ◽  
Growth Factor ◽  
Fatty Acid Synthesis ◽  
Growth Factor Receptor ◽  
Breast Tumors ◽  
Acid Synthesis ◽  
Epidermal Growth ◽  
The Brain

Abstract Brain metastases are refractory to therapies that control systemic disease in patients with human epidermal growth factor receptor 2-positive breast cancer and the brain microenvironment contributes to this therapy resistance. Nutrient availability can vary across tissues, therefore metabolic adaptations required for brain metastatic breast cancer growth may introduce liabilities that can be exploited for therapy. Here we assessed how metabolism differs between breast tumors in brain versus extracranial sites and found that fatty acid synthesis is elevated in breast tumors growing in the brain. We determine that this phenotype is an adaptation to decreased lipid availability in the brain relative to other tissues, resulting in site-specific dependency on fatty acid synthesis for breast tumors growing at this site. Genetic or pharmacological inhibition of fatty acid synthase reduces human epidermal growth factor receptor 2-positive breast tumor growth in the brain, demonstrating that differences in nutrient availability across metastatic sites can result in targetable metabolic dependencies.

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