| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5846359 | Toxicology and Applied Pharmacology | 2013 | 11 Pages |
Abstract
In conclusion, AZA induces resistance in hepatoblastoma cells to IGF-1, which leads to autophagy activation, and causes apoptosis when it is combined with bafilomycin A1. We are presenting here a novel mechanism of action of azathioprine, which could be useful in treatment of IGF-1 dependent tumors, especially in its combination with other drugs.
Keywords
NACIRSBAFEC50E2FERKFOXO1mTORE2F transcription factorGSTPARPPI3KGTPγSguanosine 5′-O-[gamma-thio]triphosphateLC33-MA3-methyladenineMAPKN-acetylcysteineAktAutophagyinsulin receptor substratebafilomycin A1thiopurineForkhead box O1Apoptosismicrotubule-associated protein light chain 3Cancerphosphoinositide-3-kinasehalf maximal effective concentrationmammalian target of rapamycinretinoblastoma proteinprotein kinase Bmitogen-activated protein kinasepoly (ADP-ribose) polymeraseSenescenceDesensitizationextracellular signal-regulated kinaseglutathione S transferase
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Authors
Borja Hernández-Breijo, Jorge Monserrat, Irene D. Román, Águeda González-RodrÃguez, Mª Dolores Fernández-Moreno, Mª Val T. Lobo, Ángela M. Valverde, Javier P. Gisbert, Luis G. Guijarro,