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. 2024 May 17;24(1):101. doi: 10.1007/s10238-024-01365-5

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© The Author(s) 2024

Open Access This 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/.

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Fig. 2 — Mechanism of action of MUC16 in ovarian cancer. Free CA125 binding MSLN inhibited DKK1 expression, activated SGK3/FOXO3a pathway, and MUC16 binding MSLN on cell surface promoted epithelial ovarian cancer metastasis. High expression of MUC16 can promote the development of ovarian cancer through Foxo3a, Bcl-2, GLUT1, E-cadherin, P120ctn/RhoA, and PI3K/AKT/pS6.CircMUC16 modulates autophagy by sponging miR-199a-5p to enhance Beclin1 and RUNX1 expression, reciprocally regulated by RUNX1, and directly interacts with ATG13 to influence ATG13 expression