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. 2021 May 1;14:62. doi: 10.1186/s13048-021-00815-y

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© The Author(s) 2021

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. 5 — Model of adipocyte-induced EOC cell proliferation through the SphK1-S1PR1/3 signalling pathway. Adipocytes induce ERK-dependent activation of SphK1, release of S1P and the consequent activation of S1PR1/3, leading to ERK phosphorylation and EOC cell proliferation. SphK1 or S1PR1/3 depletion inhibits adipocyte-induced EOC growth