Abstract
Autophagy is a lysosomal-driven catabolic process that contributes to preserve cell and tissue homeostases through the regular elimination of damaged, aged and redundant self-constituents. In normal cells, autophagy protects from DNA mutation and carcinogenesis by preventive elimination of pro-oxidative mitochondria and protein aggregates. Mutations in oncogenes and oncosuppressor genes dysregulate autophagy. Up-regulated autophagy may confer chemo- and radio-resistance to cancer cells, and also a pro-survival advantage in cancer cells experiencing oxygen and nutrient shortage. This fact is the rationale for using autophagy inhibitors along with anti-neoplastic therapies. Yet, aberrant hyper-induction of autophagy can lead to cell death, and this phenomenon could also be exploited for cancer therapy. The actual level of autophagy in the cancer cell is greatly affected by vascularization, inflammation, and stromal cell infiltration. In addition, small non-coding microRNAs have recently emerged as important epigenetic modulators of autophagy. The present review focuses on the potential involvement of macroautophagy, and on its genetic and epigenetic regulation, in ovarian cancer pathogenesis and progression.
Highlights
Ovarian cancer ranks as the fifth leading cause of cancer-related deaths among women, and the leading cause of death from gynecological cancer [1]
The difficulty to diagnose the disease at early stage and the persistence of dormant, drug-resistant cancer cells that cause relapse, are the primary reasons for the high mortality rate in ovarian cancer patients [2]
Consistent with a role of autophagy-active beclin 1 in ovarian cancer progression, we found that hyper-expression of both beclin 1 and LC3 in ovarian cancer cells was associated with a good chemotherapeutic response in patients (Peracchio et al, unpublished data; Figure 3)
Summary
Ovarian cancer ranks as the fifth leading cause of cancer-related deaths among women, and the leading cause of death from gynecological cancer [1]. Autophagy dysregulation in cancer cells has been blamed as a possible cause of dormancy and of resistance to radio- and chemotherapeutic treatments, and proteins involved in the regulation of this process are being considered as targets for anticancer molecular therapy.
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