Distant metastases are responsible for 90% of breast cancer-associated mortality, and a clear link has been established between metastatic disease and obesity-related metabolic perturbation. As more studies describe the nuances of metabolic reprogramming in various malignancies, there is growing interest in understanding the mechanistic basis of how these changes drive invasiveness and metastasis. Focusing on breast cancer, Rios Garcia et al. demonstrate that the lipogenic enzyme acetyl-CoA carboxylase 1 (ACC1) is the common target of TAK1-AMPK signaling triggered by leptin and TGF-beta binding to their receptors [1]. The subsequent ACC1 inactivation (through phosphorylation (pACC1)) leads to elevated levels of acetyl-CoA, increased acetylation of factors including Smad2, and Smad2-stimulated induction of an epithelial-mesenchymal transition (EMT) phenotype and metastasis. The authors found elevated levels of pACC1 in metastatic tissue samples from human microarrays of both breast and lung tumors, indicating that this mechanism could be relevant to many solid malignancies. Thus, this study highlights the potential utility of a “metabolocentric” approach to the prevention of breast cancer metastasis that may have broad application.
Outstanding GeneTex Antibodies for Epithelial-Mesenchymal Transition Research
High-Quality GeneTex Antibodies for Lipid Biosynthesis Research
✔ Cited and independently reviewed
✔ Validated for multiple applications: WB, ICC/IF, IHC-P, EM, IP, ELISA, ChIP
✔ Validated by Knockout/Knockdown using CRISPR- or RNAi-mediated technologies
Reference:
1. Cell Metab. 2017 Dec 5;26(6):842-855.e5.