Journal
CELL REPORTS
Volume 14, Issue 9, Pages 2154-2165Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2016.02.004
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Funding
- NIH [R21CA179720, R21CA173150, R21CA179720S1, R21CA179720S2, U54-CA149196]
- DOD [DAMD W81XWH-11-1-0292]
- DLDCC Pilot Projects
- BCM Cancer Center Grant [P30CA125123]
- DEF [NIH-R01CA184208]
- MTL [P50CA50183, R01CA112305, U54 CA149196, P01CA30195]
- AS [R21CA185516, U01CA179674]
- NP [ACS 127430-RSG-15-105-01-CNE]
- CPRIT Proteomics and Metabolomics Core Facility [RP120092]
- Cytometry and Cell Sorting Core [NIAID P30AI036211, NCRR S10RR024574]
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Transmitochondrial cybrids and multiple OMICs approaches were used to understand mitochondrial reprogramming and mitochondria-regulated cancer pathways in triple-negative breast cancer (TNBC). Analysis of cybrids and established breast cancer (BC) cell lines showed that metastatic TNBC maintains high levels of ATP through fatty acid beta oxidation (FAO) and activates Src oncoprotein through autophosphorylation at Y419. Manipulation of FAO including the knocking down of carnitine palmitoyltransferase-1A (CPT1) and 2 (CPT2), the rate-limiting proteins of FAO, and analysis of patient-derived xenograft models confirmed the role of mitochondrial FAO in Src activation and metastasis. Analysis of TCGA and other independent BC clinical data further reaffirmed the role of mitochondrial FAO and CPT genes in Src regulation and their significance in BC metastasis.
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