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. 2022 Jun 11;8:285. doi: 10.1038/s41420-022-01066-6

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© The Author(s) 2022

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. 7 — A, B ISH staining of circRFWD3(pink stain in the cytoplasm) and IHC staining of PPARγ in an HNSCC clinical cohort, scale bar, 10 μm. C, D Kaplan–Meier analysis showed that circRFWD3 and PPARγ were negatively correlated with the overall survival rate of HNSCC patients according to our clinical cohort. E, F Kaplan–Meier analysis showed that circRFWD3 and the mRNA expression of PPARγ were negatively correlated with the overall survival rate of HNSCC patients in the TCGA database. G Molecular mechanism of circRFWD3 involved in HNSCC metastasis. CircRFWD3, resulting from back-splicing of exons 7 and 8, could sponge-like bind to miR-27a/b to relieve the inhibitory effect of miR-27a/b on PPARγ, promoting the transcription and translation of PPARγ. Then, upregulated PPARγ could activate the NF-κB signaling pathway to promote the expression of MMP13 and accelerate tumor metastasis.