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. 2020 Sep 23;13:115. doi: 10.1186/s13048-020-00718-4

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — The role of adipocytes in EOC metastasis. Adipocyte-secreted cytokines, such as IL-6, IL-8, IL-11 and IL-33, induced EMT and detachment of EOC cells by inhibiting E-cadherin expression. Adipocytes affect the travel of EOC cells in the peritoneal fluid through modulating several functions including (1) ascites formation by secreting VEGF, which increases vascular permeability; (2) EOC anoikis resistance by secreting IGF-1, IL-6 and IL-8, which activate the survival pathway and EMT of EOC; (3) EOC movement by secreting MCP-1, IL-6 and IL-8, which activate the mitogenic pathway of EOC. Adipocytes affect EOC implantation through modulating (1) EOC adhesion by secreting TNF-α and HGF, which promote CD44 expression; (2) EOC invasion by secreting Leptin, which promote MMP2 expression. Together, these roles of adipocytes facilitate adipocyte-induced EOC metastasis