Fig. 1: Upregulation of TRIM22 induces cellular senescence in HCC.

A RT-qPCR of an expression profiling array (GSE30240) for IR-treated HepG2 cells. Data are presented as mean ± SD (unpaired two-tailed t-test, MIB2: **P = 0.0044, t = 5.805; PML: **P = 0.0042, t = 5.874; TRIM22: ***P = 0.0008, t = 8.990; TRIM38: **P = 0.01, t = 4.606; TRIM5: ***P = 0.0001, t = 14.34; HERC6: **P = 0.0013, t = 8.116; TRIM21: **P = 0.0016, t = 7.667; n = 3). B, C HepG2 cells were transfected with specific siRNA against each E3 ligase candidate in HepG2 cells. SA-β-Gal assay (B) (one-way ANOVA with Tukey’s multiple comparison test, F(7,16) = 21.96, ***P < 0.0001; ***P = 0.0003, n = 3) and cell counting (C) were performed. Data are presented as mean ± SD (one-way ANOVA with Tukey’s multiple comparison test, F(7,16) = 92.09, ***P < 0.0001; ***P = 0.0002, n = 3). Positive control (PC) for dead cells, Doxorubicin 2 μg/mL. D Gene expression analysis of TRIM22 and senescence-associated genes in the TCGA-LIHC database (Pearson correlation, n = 369). E–H Western blotting (E), Edu incorporation assay. Scale bars, 100 μm (F) Data are presented as mean ± SD (unpaired two-tailed t-test, HepG2: **P = 0.0059, t = 5.352, n = 3; SK-Hep-1: **P = 0.0046, t = 5.724, n = 3), cell counting (G) Data are presented as mean ± SD (unpaired two-tailed t-test, HepG2: ***P = 0.0008, t = 9.097, n = 3; SK-Hep-1: **P = 0.0020, t = 7.168, n = 3), and SA-β-Gal assay (H) Data are presented as mean ± SD (unpaired two-tailed t-test, HepG2: ***P < 0.0001, t = 23.00, n = 3; SK-Hep-1: **P = 0.0012, t = 8.265, n = 3) were performed in TRIM22-overexpressing HepG2 and SK-Hep-1 HCC cells.