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oai:docta.ucm.es:20.500.14352/983792024-10-07T23:51:24Zcom_20.500.14352_14col_20.500.14352_15

Piñeiro, David Martín, Elena Guerra Pérez, Natalia Salinas, Matilde González, Victor 2024-02-02T14:59:37Z 2024-02-02T14:59:37Z 2007 Piñeiro, David, et al. «Calpain Inhibition Stimulates Caspase-Dependent Apoptosis Induced by Taxol in NIH3T3 Cells». Experimental Cell Research, vol. 313, n.o 2, enero de 2007, pp. 369-79. https://doi.org/10.1016/j.yexcr.2006.10.020. 0014-4827 10.1016/j.yexcr.2006.10.020 https://hdl.handle.net/20.500.14352/98379 1090-2422 https://doi.org/10.1016/j.yexcr.2006.10.020 Taxol is an anticancer drug that triggers apoptosis in a wide spectrum of cancers such as ovarian, breast, lung, head and neck, and bladder carcinoma by both caspase-dependent and -independent apoptosis mechanisms. However, the exact signaling pathways involved in taxol-induced apoptosis strongly depend on the cellular background and they are not completely established yet. In this study we demonstrate that taxol induces caspase-3- independent apoptosis in NIH3T3 cells by a calpain-mediated mechanism. Taxol treatment produced changes in the mitochondrial membrane potential (ΔΨm) which could be responsible of Ca2+ release from the mitochondria and the consequent calpain activation. Interestingly, we show that calpain produced proteolysis of caspase-3 and demonstrate that, accordingly, calpain inhibition increased taxol-induced apoptosis. In addition, we reveal that poly (ADP-ribose) polymerase (PARP) was processed by calpain in taxol-treated cells and by caspase-3 after calpain inhibition. In conclusion, these results demonstrate for the first time that calpain could play an important role modulating taxol-induced apoptosis. Further studies are needed to address the potentiality of inducing apoptosis by a combined use of taxol and calpain inhibitors in cells with increased calpain activity. eng restricted access Calpain inhibition stimulates caspase-dependent apoptosis induced by taxol in NIH3T3 cells journal article