ADAR1 promotes liver cancer progression via post-transcriptional regulation of PPARγ (IMAGE)
Caption
(A) PPARγ protein expression levels in HepG2 cells following ADAR1 overexpression. (B) PPARγ protein expression levels in HepG2 cells following ADAR1 knockdown. (C) PPARγ mRNA expression levels in HepG2 cells following ADAR1 overexpression. (D) PPARγ mRNA expression levels in HepG2 cells following ADAR1 knockdown. (E) Correlation analysis between ADAR1 and PPARγ expression (r = 0.38; GEPIA database). (F) RNA immunoprecipitation assay confirmed specific binding of ADAR1 protein to PPARγ mRNA. (G) Analysis of the GEPIA database demonstrating relative PPARγ levels in hepatocellular carcinoma (HCC) tumor tissues (red box, n = 369) versus normal liver tissues (gray box, n = 160). (H) Overall survival analysis of HCC patients stratified by PPARγ expression levels in the GEPIA database. (I) PPARγ protein expression levels in paired clinical HCC tumor tissues (T) and adjacent non-tumor tissues (N) (n = 8). All experiments were performed with at least three biologically independent replicates (n ≥ 3). Data were presented as mean ± standard error of the mean. Statistical significance was determined using Student's two-tailed t-test for two-group comparisons or one-way ANOVA for multiple groups. ∗∗p < 0.01, ∗∗∗p < 0.001.
Credit
Jing Liu, Yongle Zhao, Xue Gong, Lin Yuan, Shengyong Yang, Wenwen Jian, Han Yan, Honglin Chen, Zhicheng Yang, Yiheng Sun, Tianle Gu, He Lu, Hongyun Zhao, Zeng Tu
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