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. 2022 Nov 4;15:161. doi: 10.1186/s13045-022-01381-6

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© The Author(s) 2022

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. 7 — RIG-I expression and methylation may be correlated to human hepatocarcinogenesis, prognosis, and NAFLD progression. a RIG-I, JMJD4, and STAT3 phosphorylation were examined in human normal liver tissues and dysplastic nodule tissues from the indicated patients. b Quantified RIG-I expression and STAT3 phosphorylation in human normal liver (N) tissues and dysplastic nodule (DN) tissues were shown (n = 12, unpaired t-test). c The correlation between RIG-I expression and STAT3 phosphorylation in human dysplastic nodule tissues was analyzed by Pearson’s correlation coefficient assay. d Quantified JMJD4 protein level in human normal liver (N) tissues and dysplastic nodule (DN) tissues were shown (n = 12, unpaired t-test). e Kaplan–Meier survival curves of overall survival based on dichotomized RIG-I and JMJD4 mRNA expression in HCC tissues of Cohort 1 and 2. The median levels of RIG-I and JMJD4 expression in each cohort were used as the cutoff, with log-rank test for significance. f RIG-I, JMJD4, and HMGCR phosphorylation were examined in human normal liver tissues and NAFLD tissues from the indicated patients. g Methylated RIG-I at K18 or K146 were examined in the precipitates using RIG-I antibody from human normal liver tissues and NAFLD tissues as in f. h, i Quantified RIG-I protein level (h) and HMGCR phosphorylation level (i) in human normal liver tissues (N, n = 12) and the indicated NAFLD tissues (n = 8, unpaired t-test) were shown. j Serum TC of the indicated NAFLD patients were shown (n = 8, unpaired t-test). k The correlation between RIG-I expression and HMGCR phosphorylation in human NAFLD tissues was analyzed by Pearson’s correlation coefficient assay. l Quantified JMJD4 protein level in human normal liver (N, n = 12) tissues and NAFLD (n = 16, unpaired t-test) tissues were shown. m Working model for the mechanism of constitutive methylated RIG-I at K18 and K146 inhibits HMGCR phosphorylation to promote cholesterol synthesis and NAFLD progression, while IL-6-induced and JMJD4-mediated RIG-I demethylation inhibits STAT3 phosphorylation to suppress hepatocarcinogenesis, and decreased RIG-I in HcPCs enhances IL-6 effects and drives them to established HCC. Data are shown as mean ± s.d., survival curves, or photographs as indicated