Essentiality of fatty acid synthase in the 2D to anchorage-independent growth transition in transforming cells

Upregulation of fatty acid synthase (FASN) is a common event in cancer, although its mechanistic and potential therapeutic roles are not completely understood. In this study, we establish a key role of FASN during transformation. FASN is required for eliciting the anaplerotic shift of the Krebs cycl...

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Detalles Bibliográficos
Autores: Bueno, Maria J, Jimenez-Renard, Veronica, Samino, Sara, Capellades, Jordi, Junza, Alejandra, López-Rodríguez, María Luz, Garcia-Carceles, Javier, Lopez-Fabuel, Irene, Bolaños, Juan P, Chandel, Navdeep S, Yanes, Oscar, Colomer, Ramon, Quintela Fandino, Miguel Angel
Tipo de recurso: artículo
Fecha de publicación:2019
País:España
Institución:Instituto de Salud Carlos III (ISCIII)
Repositorio:Repisalud
Idioma:inglés
OAI Identifier:oai:repisalud.isciii.es:20.500.12105/9317
Acceso en línea:http://hdl.handle.net/20.500.12105/9317
Access Level:acceso abierto
Palabra clave:Animals
Cell Line
Cells, Cultured
Embryo, Mammalian
Embryonic Stem Cells
Fatty Acid Synthases
Fatty Acids
Female
Fibroblasts
HEK293 Cells
Humans
Male
Mice, Inbred C57BL
Mice, Knockout
Mice, Nude
Mice, Transgenic
Neoplasms, Experimental
Tumor Burden
Descripción
Sumario:Upregulation of fatty acid synthase (FASN) is a common event in cancer, although its mechanistic and potential therapeutic roles are not completely understood. In this study, we establish a key role of FASN during transformation. FASN is required for eliciting the anaplerotic shift of the Krebs cycle observed in cancer cells. However, its main role is to consume acetyl-CoA, which unlocks isocitrate dehydrogenase (IDH)-dependent reductive carboxylation, producing the reductive power necessary to quench reactive oxygen species (ROS) originated during the switch from two-dimensional (2D) to three-dimensional (3D) growth (a necessary hallmark of cancer). Upregulation of FASN elicits the 2D-to-3D switch; however, FASN's synthetic product palmitate is dispensable for this process since cells satisfy their fatty acid requirements from the media. In vivo, genetic deletion or pharmacologic inhibition of FASN before oncogenic activation prevents tumor development and invasive growth. These results render FASN as a potential target for cancer prevention studies.