Nanomaterials and Autophagy: New Insights in Cancer Treatment
AbstractAutophagy represents a cell’s response to stress. It is an evolutionarily conserved process with diversified roles. Indeed, it controls intracellular homeostasis by degradation and/or recycling intracellular metabolic material, supplies energy, provides nutrients, eliminates cytotoxic materials and damaged proteins and organelles. Moreover, autophagy is involved in several diseases. Recent evidences support a relationship between several classes of nanomaterials and autophagy perturbation, both induction and blockade, in many biological models. In fact, the autophagic mechanism represents a common cellular response to nanomaterials. On the other hand, the dynamic nature of autophagy in cancer biology is an intriguing approach for cancer therapeutics, since during tumour development and therapy, autophagy has been reported to trigger both an early cell survival and a late cell death. The use of nanomaterials in cancer treatment to deliver chemotherapeutic drugs and target tumours is well known. Recently, autophagy modulation mediated by nanomaterials has become an appealing notion in nanomedicine therapeutics, since it can be exploited as adjuvant in chemotherapy or in the development of cancer vaccines or as a potential anti-cancer agent. Herein, we summarize the effects of nanomaterials on autophagic processes in cancer, also considering the therapeutic outcome of synergism between nanomaterials and autophagy to improve existing cancer therapies.
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Panzarini, E.; Inguscio, V.; Tenuzzo, B.A.; Carata, E.; Dini, L. Nanomaterials and Autophagy: New Insights in Cancer Treatment. Cancers 2013, 5, 296-319.
Panzarini E, Inguscio V, Tenuzzo BA, Carata E, Dini L. Nanomaterials and Autophagy: New Insights in Cancer Treatment. Cancers. 2013; 5(1):296-319.Chicago/Turabian Style
Panzarini, Elisa; Inguscio, Valentina; Tenuzzo, Bernardetta A.; Carata, Elisabetta; Dini, Luciana. 2013. "Nanomaterials and Autophagy: New Insights in Cancer Treatment." Cancers 5, no. 1: 296-319.