Oleic acid promotes migration on MDA-MB-231 breast cancer cells through an arachidonic acid-dependent pathway |
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| Authors: | Napoleon Navarro-Tito Adriana Soto-Guzman Luis Castro-Sanchez Raul Martinez-Orozco Eduardo Perez Salazar |
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| Institution: | 1. Nano Characterization Unit, National Institute for Materials Science, 1-2-1 Sengen, Tsukuba, Ibaraki 305-0047, Japan;2. Vortex Dynamics Group, National Institute for Materials Science, 1-2-1 Sengen, Tsukuba, Ibaraki 305-0047, Japan;3. Materials and Nano-architectronics, National Institute for Materials Science, 1-2-1 Sengen, Tsukuba, Ibaraki 305-0047, Japan;4. Surface Characterization Group, Nano Characterization Unit Advanced Key Technologies Division, National Institute for Materials Science, 1-2-1 Sengen, Main Bldg, Room-815 Tsukuba, 305-0047, Japan;1. Centre for Lipid Research & Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, 400016, Chongqing, China;2. The Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases (CCID), Zhejiang University, 310058, Hangzhou, China;3. John Moorhead Research Laboratory, Centre for Nephrology, University College London Medical School, Royal Free Campus, University College London, London, NW3 2PF, United Kingdom;1. James Paget University Hospital, Great Yarmouth, Norfolk, UK;2. Institute of Public Health, University of Cambridge, UK;3. Norwich Medical School, University of East Anglia, Norwich, UK;1. Department of Cell Biology, CINVESTAV-IPN, Mexico City, 07360, Mexico;2. First October Regional Hospital-ISSSTE, Mexico City, 07760, Mexico |
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| Abstract: | An association between dietary fatty, obesity and an increased risk of developing breast cancer has been suggested. In breast cancer cells, free fatty acids (FFAs) mediate biological effects including cell proliferation and ERK1/2 activation. However, the contribution of FFAs to tumor progression and metastasis through the regulation of cell migration has not been studied. We demonstrated here that stimulation on MDA-MB-231 breast cancer cells with oleic acid (OA) promotes an increase in focal adhesion kinase (FAK) phosphorylation, as revealed by site-specific antibodies that recognize the phosphorylation state of FAK at tyrosine-397 (Tyr-397), Tyr-577 and in vitro kinase assays. OA also promotes the migration of MDA-MB-231 cells. Treatment with Gi/Go proteins, phospholipase C (PLC), lipoxygenases (LOXs) and Src inhibitor prevents FAK phosphorylation and cell migration. In summary, our findings delineate a new signal transduction pathway, where OA mediates the production of arachidonic acid (AA), and then AA metabolites mediate FAK phosphorylation and cell migration in MDA-MB-231 breast cancer cells. |
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