A link between lipid metabolism and epithelial-mesenchymal transition provides a target for colon cancer therapy
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A link between lipid metabolism and epithelial-mesenchymal transition provides a target for colon cancer therapy. / Sánchez-Martínez, Ruth; Cruz-Gil, Silvia; Cedrón, Marta Gómez de; Álvarez-Fernández, Mónica; Vargas, Teodoro; Molina, Susana; García, Belén; Herranz, Jesús; Moreno-Rubio, Juan; Reglero, Guillermo; Perez-Moreno, Mirna; Feliu, Jaime; Malumbres, Marcos; Molina, Ana Ramírez de.
In: OncoTarget, Vol. 6, No. 36, 2015, p. 38719-36.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - A link between lipid metabolism and epithelial-mesenchymal transition provides a target for colon cancer therapy
AU - Sánchez-Martínez, Ruth
AU - Cruz-Gil, Silvia
AU - Cedrón, Marta Gómez de
AU - Álvarez-Fernández, Mónica
AU - Vargas, Teodoro
AU - Molina, Susana
AU - García, Belén
AU - Herranz, Jesús
AU - Moreno-Rubio, Juan
AU - Reglero, Guillermo
AU - Perez-Moreno, Mirna
AU - Feliu, Jaime
AU - Malumbres, Marcos
AU - Molina, Ana Ramírez de
PY - 2015
Y1 - 2015
N2 - The alterations in carbohydrate metabolism that fuel tumor growth have been extensively studied. However, other metabolic pathways involved in malignant progression, demand further understanding. Here we describe a metabolic acyl-CoA synthetase/stearoyl-CoA desaturase ACSL/SCD network causing an epithelial-mesenchymal transition (EMT) program that promotes migration and invasion of colon cancer cells. The mesenchymal phenotype produced upon overexpression of these enzymes is reverted through reactivation of AMPK signaling. Furthermore, this network expression correlates with poorer clinical outcome of stage-II colon cancer patients. Finally, combined treatment with chemical inhibitors of ACSL/SCD selectively decreases cancer cell viability without reducing normal cells viability. Thus, ACSL/SCD network stimulates colon cancer progression through conferring increased energetic capacity and invasive and migratory properties to cancer cells, and might represent a new therapeutic opportunity for colon cancer treatment.
AB - The alterations in carbohydrate metabolism that fuel tumor growth have been extensively studied. However, other metabolic pathways involved in malignant progression, demand further understanding. Here we describe a metabolic acyl-CoA synthetase/stearoyl-CoA desaturase ACSL/SCD network causing an epithelial-mesenchymal transition (EMT) program that promotes migration and invasion of colon cancer cells. The mesenchymal phenotype produced upon overexpression of these enzymes is reverted through reactivation of AMPK signaling. Furthermore, this network expression correlates with poorer clinical outcome of stage-II colon cancer patients. Finally, combined treatment with chemical inhibitors of ACSL/SCD selectively decreases cancer cell viability without reducing normal cells viability. Thus, ACSL/SCD network stimulates colon cancer progression through conferring increased energetic capacity and invasive and migratory properties to cancer cells, and might represent a new therapeutic opportunity for colon cancer treatment.
KW - Cell Line, Tumor
KW - Cell Movement
KW - Cell Proliferation
KW - Coenzyme A Ligases
KW - Colonic Neoplasms
KW - Epithelial-Mesenchymal Transition
KW - HEK293 Cells
KW - Humans
KW - Lipid Metabolism
KW - Neoplasm Invasiveness
KW - Signal Transduction
KW - Stearoyl-CoA Desaturase
KW - Journal Article
KW - Research Support, Non-U.S. Gov't
U2 - 10.18632/oncotarget.5340
DO - 10.18632/oncotarget.5340
M3 - Journal article
C2 - 26451612
VL - 6
SP - 38719
EP - 38736
JO - Oncotarget
JF - Oncotarget
SN - 1949-2553
IS - 36
ER -
ID: 188368268