| Literature DB >> 26923594 |
Jun Hyoung Park1, Sajna Vithayathil1, Santosh Kumar1, Pi-Lin Sung2, Lacey Elizabeth Dobrolecki3, Vasanta Putluri4, Vadiraja B Bhat5, Salil Kumar Bhowmik4, Vineet Gupta1, Kavisha Arora1, Danli Wu6, Efrosini Tsouko7, Yiqun Zhang8, Suman Maity4, Taraka R Donti1, Brett H Graham1, Daniel E Frigo9, Cristian Coarfa4, Patricia Yotnda6, Nagireddy Putluri4, Arun Sreekumar10, Michael T Lewis11, Chad J Creighton8, Lee-Jun C Wong12, Benny Abraham Kaipparettu13.
Abstract
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 β 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.Entities:
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Year: 2016 PMID： 26923594 PMCID： PMC4809061 DOI： 10.1016/j.celrep.2016.02.004
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423