Abstract
Ovarian cancer (OC) is one of the three types of malignant tumors in the female reproductive system, and epithelial ovarian cancer (EOC) is its most typical form. Due to the asymptomatic nature of the early stages and resistance to chemotherapy, EOC has both a poor prognosis and a high fatality rate. Current treatments for OC are very limited, and the 5-years survival rate is approximately 30%. Exosomes, which are microvesicles ranging from approximately 30–100 nm in size that are secreted by living cells, can be produced from different cell types and detected in various body fluids. Cancer cells can secrete more exosomes than healthy cells, and more importantly, the content of cancer cell-derived exosomes is distinct. The exosomes shedding from tumor cells are considered to be involved in tumor progression and metastasis. As such, exosomes are expected to be potential tools for tumor diagnosis and treatment. In this review, we briefly present the emerging roles of exosomes in OC and summarize related articles about their roles as diagnostic or prognostic biomarkers and in the treatment and drug resistance of OC.
Highlights
Epithelial ovarian cancer (EOC) is one of the most malignant tumors in the female reproductive system
We briefly present the emerging roles of exosomes in OC and summarize related articles about their roles as diagnostic or prognostic biomarkers and in the treatment and drug resistance of OC, especially EOC
Exosome shedding, which is frequently observed in tumor cells, is suggested to be involved in several aspects of tumor progression. It demonstrated that exosomes isolated from invasive tumor cell lines as well as the bodily fluids of OC patients can deliver membrane-type 1 matrix metalloprotease (MT1-MMP), which is involved in matrix degradation and disease progression [58]
Summary
Epithelial ovarian cancer (EOC) is one of the most malignant tumors in the female reproductive system. MiR-222-3p can transfer from EOC cells to macrophages by exosomes, thereby effectively regulating the polarization of tumor-promoting M2 macrophages [22].
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