Research
05 Oct 2016
Metabolic block improves antitumor therapies
A new study lead by Marcos Malumbres and Maria Salazar-Roa (CNIO) with the participation of Eduardo Rial and Patricia Boya groups at CIB, has been publisehd in Nature Cell Biology.
The work shows that one key point for cancerous cell survival during mitotic arrest is a change in the energetic metabolism, such as the energy is obtained by anaerobic glycolisis. This metabolic change includes activation of the AMPK sensor, induction of the expression of PFKFB3, the glycolisis regulator, and the elimination of mithocondria by autophagy. Using cell models for breast cancer and mice, authors show that therapy with antimitotic drugs, like taxol, is more efficient in combination with PFKFB3 inhibitors. Rial's group shows that the inhibition of mithocondrial respiration after mitosis stops, and Lorena Esteban-Martínez, Esther Seco and Patricia Boya demonstrated that for the methabolic change to take place it is essential the elimination of mithocondria by mitophagy.