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Review
. 2021 Sep 18;9(9):1257.
doi: 10.3390/biomedicines9091257.

The Role and Clinical Interest of Extracellular Vesicles in Pregnancy and Ovarian Cancer

Affiliations
Review

The Role and Clinical Interest of Extracellular Vesicles in Pregnancy and Ovarian Cancer

Nazanin Yeganeh Kazemi et al. Biomedicines. .

Abstract

Ovarian cancer and pregnancy are two states in which the host immune system is exposed to novel antigens. Indeed, both the tumor and placenta must invade tissues, remodel vasculature to establish a robust blood supply, and evade detection by the immune system. Interestingly, tumor and placenta tissue use similar mechanisms to induce these necessary changes. One mediator is emerging as a key player in invasion, vascular remodeling, and immune evasion: extracellular vesicles (EVs). Many studies have identified EVs as a key mediator of cell-to-cell communication. Specifically, the cargo carried by EVs, which includes proteins, nucleic acids, and lipids, can interact with cells to induce changes in the target cell ranging from gene expression to migration and metabolism. EVs can promote cell division and tissue invasion, immunosuppression, and angiogenesis which are essential for both cancer and pregnancy. In this review, we examine the role of EVs in ovarian cancer metastasis, chemoresistance, and immune modulation. We then focus on the role of EVs in pregnancy with special attention on the vascular remodeling and regulation of the maternal immune system. Lastly, we discuss the clinical utility of EVs as markers and therapeutics for ovarian cancer and pre-eclampsia.

Keywords: angiogenesis; exosome; extracellular vesicle; immune modulation; invasion; ovarian cancer; placenta; preeclampsia; pregnancy; syncytial knot.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Characteristics of extracellular vesicles based on size, surface marker expression, origin, and cargo.
Figure 2
Figure 2
Mechanisms of invasion, growth, and chemoresistance in ovarian cancer mediated by tumor-derived extracellular vesicles.
Figure 3
Figure 3
Effects of EVs on different cell types in PE.

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