Piñeiro, DavidGonzález, Víctor MSalinas, MatildeMartín, M. ElenaHernández Jiménez, Macarena2024-02-072024-02-072007-10Piñeiro D, González VM, Hernández-Jiménez M, Salinas M, Martín ME. Translation regulation after taxol treatment in NIH3T3 cells involves the elongation factor (eEF)2. Exp Cell Res. 2007 Oct 15;313(17):3694-706. doi: 10.1016/j.yexcr.2007.07.025. Epub 2007 Aug 1. PMID: 17825817.0014-482710.1016/j.yexcr.2007.07.025https://hdl.handle.net/20.500.14352/100013Changes to the translational machinery that occur during apoptosis have been described in the last few years. The two principal ways in which translational factors are modified during apoptosis are: (i) changes in protein phosphorylation and (ii) specific proteolytic cleavages. Taxol, a member of a new class of anti-tubulin drugs, is currently used in chemotherapeutic treatments of different types of cancers. We have previously demonstrated that taxol induces calpain-mediated apoptosis in NIH3T3 cells [Piñeiro et al., Exp. Cell Res., 2007, 313:369–379]. In this study we found that translation was significantly inhibited during taxol-induced apoptosis in these cells. We have studied the phosphorylation status and expression levels of eIF2a, eIF4E, eIF4G and the regulatory protein 4E-BP1, all of which are implicated in translation regulation. We found that taxol treatment did not induce changes in eIF2α phosphorylation, but strongly decreased eIF4G, eIF4E and 4E-BP1 expression levels. MDL28170, a specific inhibitor of calpain, prevented reduction of eIF4G, but not of eIF4E or 4E-BP1 levels. Moreover, the calpain inhibitor did not block taxol-induced translation inhibition. All together hese findings demonstrated that none of these factors are responsible for the taxol-induced protein synthesis inhibition. On the contrary, taxol treatment increased elongation factor eEF2 phosphorylation in a calpain-independent manner, supporting a role for eEF2 in taxol-induced translation inhibition.engAttribution-NonCommercial-NoDerivatives 4.0 Internationalhttp://creativecommons.org/licenses/by-nc-nd/4.0/journal articlehttps://www.sciencedirect.com/science/article/pii/S0014482707003618?via%3Dihubrestricted access61:17ApoptosiseEF2Initiation factorsTaxolTranslationCiencias Biomédicas32 Ciencias Médicas