The reciprocal interplay of
cancer cells and host cells is an indispensable prerequisite for
tumor growth and progression. Cells of both the innate and adaptive immune system, in particular tumor-associated macrophages (TAMs) and T cells, as well as cancer-associated fibroblasts enter into a malicious liaison with
tumor cells to create a
tumor-promoting and immunosuppressive tumor microenvironment (TME).
Ovarian cancer, the most lethal of all gynecological
malignancies, is characterized by a unique TME that enables specific and efficient metastatic routes, impairs immune surveillance, and mediates
therapy resistance. A characteristic feature of the
ovarian cancer TME is the role of resident host cells, in particular activated mesothelial cells, which line the peritoneal cavity in huge numbers, as well as adipocytes of the omentum, the preferred site of metastatic lesions. Another crucial factor is the peritoneal fluid, which enables the transcoelomic spread of
tumor cells to other pelvic and peritoneal organs, and occurs at more advanced stages as a
malignancy-associated effusion. This
ascites is rich in
tumor-promoting soluble factors, extracellular vesicles and detached
cancer cells as well as large numbers of T cells, TAMs, and other host cells, which cooperate with resident host cells to support
tumor progression and immune evasion. In this review, we summarize and discuss our current knowledge of the cellular and molecular interactions that govern this interplay with a focus on signaling networks formed by
cytokines,
lipids, and extracellular vesicles; the pathophysiologial roles of TAMs and T cells; the mechanism of transcoelomic
metastasis; and the cell type selective processing of signals from the TME.