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. 2020 Aug 15;20:395. doi: 10.1186/s12935-020-01479-2

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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. 5 — miR-502-5p targets PD-L1 via CD40/STAT3 pathway. a Bioinformatics predication of interaction between miR-502-5p and CD40 or STAT3. b Luciferase reporter assay showed that miR-502-5p overexpression significantly repressed the luciferase activity of CD40-wt and STAT3-wt, while the luciferase activities of CD40-mut and STAT3-mut were not affected in SGC7901 cells. c The expressions of CD40 and STAT3 determined by qRT-PCR in two gastric cancer cell lines were significantly decreased following miR-502-5p transfection. d, e After transfection with siRNA against CD40 (si-CD40) or siRNA against STAT3 (si-STAT3) for 24 h, total cellular lysates were collected and subjected to the western blot analysis with indicated antibodies. The knockdown efficiency of si-CD40 or si-STAT3 was determined by qRT-PCR. f Chromatin immunoprecipitation (ChIP) assay was performed in SGC7901 cells using the STAT3 antibody. The IgG antibody served as a negative control. Analysis was conducted using specific primers for the promoter region of PD-L1