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. 2019 Sep 18;38:411. doi: 10.1186/s13046-019-1394-6

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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.

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Fig. 7 — The schematic diagram depicts the regulatory mechanism of HOTTIP in the immune escape of OC cells. In OC cells, high expression of HOTTIP can enhance the expression and secretion of IL-6 from OC cells by promoting the transcription of IL-6. The secreted IL-6 stimulates the expression of PD-L1 by binding to the IL-6 receptor on the surface of neutrophils around the cancer cells and then activates the STAT3 pathway, thus increasing the expression of PD-L1 on the surface of neutrophils and inhibiting the activity of T cells, which further promotes apoptosis, thus facilitating the immune escape of OC cells