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. 2022 May 13;18(8):3470–3483. doi: 10.7150/ijbs.73398

Figure 2.

Figure 2

Histone lactylation is caused by VHL inactivation and its association with clinical outcomes. (A) Western blot showing histone global lactylation and H3K18la levels in WT (-) and VHL-reconstituted (+) 786-O and A498 cells. (B) Western blot showing histone global lactylation and H3K18la levels in Caki-1 cells with or without VHL knockdown. (C) Western blot showing histone global lactylation and H3K18la levels in 786-O and A498 cells with or without HIF-1α and HIF-2α knockdown. (D) Global lactylation levels at different AJCC stages. There were 10 ccRCC samples in T1 stage, 10 in T2 stage, 18 in T3 stage, and 12 in T4 stage. (E, F) Kaplan-Meier analysis of overall survival (E) and disease-free survival (F) in ccRCC patients with low (n = 18) and high (n = 32) global lactylation levels. (G) H3K18la levels at different AJCC stages. There were 10 ccRCC samples in T1 stage, 10 in T2 stage, 18 in T3 stage, and 12 in T4 stage. (H, I) Kaplan-Meier analysis of overall survival (H) and disease-free survival (I) in ccRCC patients with low (n=20) and high (n=30) H3K18la levels. Data are presented as mean±SD. *p<0.05, **p<0.01, ***p<0.001, by 1-way ANOVA (D, G) or Log-rank test (E, F, H, I).