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. 2021 May 22;12(6):528. doi: 10.1038/s41419-021-03820-7

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© The Author(s) 2021

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — A Scheme for binding sequence and sites of PPARG2 binding to the transcription factor-binding site near the AKAP12 gene promoter region. TSS, transcription start site. B ChIP assay revealing the direct binding of PPARG2 to the AKAP12 gene promoter in PC3 cells between the EV and PPARG2 group. The enriched DNA fragments within the AKAP12 gene promoter using IgG and an anti-PPARG2 antibody were amplified by PCR. Total input was used as a positive control. *P < 0.05, **P < 0.01 vs. EV group. C Serially truncated and mutated AKAP12 gene promoter constructs were co-transfected with siPPARG2 or siControl into PC3 cells, and the relative luciferase activities were determined. *P < 0.05 vs. siControl group. D Proposed graphic model for PPARG2-AKAP12 axis-mediated epigenetic regulation mechanism of proliferation, migration, and invasion in PCA cells.