2026-04-13T04:11:20Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/1056332025-12-04T19:31:21Zcom_2072_1057col_2072_478908col_2072_478917

00925njm 22002777a 4500 dc Slebe, Felipe author Rojo, Federico author Vinaixa Crevillent, Maria author García Rocha, Mar author Testoni, Giorgia author Guiu, Marc author Planet, Evarist author Samino Gené, Sara author Arenas, Enrique J. author Beltran, Antoni author Rovira, Ana author Lluch Hernández, Ana author Salvatella i Giralt, Xavier author Yanes, Oscar author Albanell Mestres, Joan author Guinovart, Joan J. (Joan Josep), 1947- author Gomis i Cabré, Roger author 2017-01-16T10:47:14Z 2017-01-16T10:47:14Z 2016-04-05 2017-01-05T09:14:02Z The mechanisms that allow breast cancer (BCa) cells to metabolically sustain rapid growth are poorly understood. Here we report that BCa cells are dependent on a mechanism to supply precursors for intracellular lipid production derived from extracellular sources and that the endothelial lipase (LIPG) fulfils this function. LIPG expression allows the import of lipid precursors, thereby contributing to BCa proliferation. LIPG stands out as an essential component of the lipid metabolic adaptations that BCa cells, and not normal tissue, must undergo to support high proliferation rates. LIPG is ubiquitously and highly expressed under the control of FoxA1 or FoxA2 in all BCa subtypes. The downregulation of either LIPG or FoxA in transformed cells results in decreased proliferation and impaired synthesis of intracellular lipids. Càncer de mama Hidrolases Biologia molecular Factors de transcripció Breast cancer Hydrolases Molecular biology Transcription factors FoxA and LIPG endothelial lipase control the uptake of extracellular lipids for breast cancer growth