Abstract
The manipulation of autophagy for cancer therapy has gained recent interest in clinical settings. Although inhibition of autophagy is currently being used in clinical trials for the treatment of several malignancies, autophagy has been shown to have diverse implications for normal cell homeostasis, cancer cell survival, and signaling to cells in the tumor microenvironment. Among these implications and of relevance for cancer therapy, the autophagic process is known to be involved in the regulation of protein secretion, in tumor cell immunogenicity, and in the regulation of epithelial-to-mesenchymal transition (EMT), a critical step in the process of cancer cell invasion. In this work, we have reviewed recent evidence linking autophagy to the regulation of EMT in cancer and normal epithelial cells, and have discussed important implications for the manipulation of autophagy during cancer therapy.
Highlights
Autophagy is a catabolic process occurring continually in eukaryotic cells at basal levels in which damaged or long-lived protein aggregates, organelles, and lipids are degraded
Autophagy has been shown to be required for cancer cell survival to metabolic stress within the tumor and for cancer cell survival to therapy, and some tumor cells with particular mutations are known to be dependent on autophagy for survival, highlighting the need to incorporate this concept into clinical trial design [3] and underscoring the need for careful selection of the cancer types or of patients in which autophagy therapies should be used
Cells [35], indicating that the tumor progression decreased after concomitant deletion of p62 in the Atg7 background, indicating inhibition of autophagy could have a detrimental effect on cancer therapy, in those treatments that p62 accumulation occurring due to autophagy inhibition played a major role in the promotion where the anti-tumoral immune response has an important role
Summary
Autophagy is a catabolic process occurring continually in eukaryotic cells at basal levels in which damaged or long-lived protein aggregates, organelles, and lipids are degraded. Autophagy has been shown to be required for cancer cell survival to metabolic stress within the tumor and for cancer cell survival to therapy, and some tumor cells with particular mutations are known to be dependent on autophagy for survival, highlighting the need to incorporate this concept into clinical trial design [3] and underscoring the need for careful selection of the cancer types or of patients in which autophagy therapies should be used In this regard, autophagy has been implicated in protein secretion [4], in the regulation of immunogenicity [5], and in tumor cell invasion. We have analyzed the evidence that autophagy inhibition by itself, or in combination with other cancer therapies, has been shown to promote malignancy in several types of cancer, with an emphasis on the promotion of EMT, suggesting that careful selection of the patients and cancer types in which autophagy should be manipulated is needed for an optimal targeting of autophagy for cancer therapy
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