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Cys-Gly) promote oxidative process, by participating in metal ion-mediated reactions membrane-bound by GGT activity, eventually leading to formation of ROS and free radicals.[112] Extracellular breakdown of glutathione by GGT, and the consequent release of the highly reactive dipeptide thiol Cys-Gly is likely to be a major determinant of protection exhibited by glutathione cisplastin nephrotoxicity.[125] Studies have further identified membrane-bound GGT activity as a factor of drug resistance, in normal and cancer cells.[126] Cells expressing sufficient GGT activity at their surface might be able to effect ‘extracellular detoxification’ of electrophilic drugs.[112] Transcription factor “NF (erythroid-derived 2)-like 2 (NFE2-L2 or NFE2-related-factor-2 [Nrf2])” is a master regulator of the AO response that modulate the expression of hundreds of genes controlling various immune and inflammatory responses, carcinogenesis and metastasis, tissue remodeling and fibrosis, and cognitive dysfunction and addictive behavior.[126] Nrf2, a positive regulator of the human AO response element (ARE), develops expression of AO enzyme such as NADPH: Quinone oxidoreductase 1.[127] Itoh et al .[128] described the mechanism of Nrf2 activation that involve a protein Keap1 which is a suppressor protein anchored in the cytoplasm that physically binds Nrf2, thus preventing its translocation to the nucleus and its access to ARE containing promoters

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The present review aims to highlight the interaction between autophagy and DOX resistance, providing the molecular machinery of autophagy and its control by genetic factors, microenvironmental factors and non-coding RNAs