Abstract
Background: Triple negative breast cancer (TNBC) is a clinically aggressive subtype of breast cancer that is associated with the over-expression of oncogenic transcription factor c-MYC (MYC). MYC drives cell growth by increasing proliferation, metabolism, and protein synthesis. Overexpression of MYC is also linked to tumor immune evasion. Because clinical-grade small molecule inhibitors against MYC remain elusive, our lab and others have worked to understand ways to therapeutically target MYC-specific cellular processes. Our group discovered that fatty acid oxidation (FAO) is an important source of energy production in TNBC, and disruption of fatty acid oxidation leads to cell death in MYC over-expressing TNBC tumors, but not in tumors with low MYC expression. Critically, how FAO inhibition specifically changes cellular signaling in MYC high tumors is unknown.
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