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. 2021 Mar 16;22:85. doi: 10.1186/s13059-021-02308-z

Fig. 8.

Fig. 8

Silencing PER1 and TP53 abolished the YTHDF2 knockdown effect. a Western blot showed that PER1 and TP53 was silenced in YTHDF2 knockdown ocular melanoma cells. b, c The effect of PER1 and TP53 silencing on proliferation of YTHDF2 knockdown OCM1 (b) and CRMM1 (c) cells was analyzed using CCK8 assay. *p < 0.05. d The effect of PER1 and TP53 silencing on tumor growth of YTHDF2 knockdown OCM1 and CRMM1 cells was evaluated by colony formation assay. e Statistical analysis of the colony formation assay performed using YTHDF2 knockdown OCM1 and CRMM1 cells with or without PER1 and TP53 silencing. All of the experiments were performed in triplicate, and relative colony numbers are shown as means ± SD. *p < 0.05. f The effect of PER1 and TP53 silencing on the migratory ability of YTHDF2 knockdown OCM1 and CRMM1 cells was evaluated by transwell assay. g Statistical analysis of cells in the transwell assay performed using YTHDF2 knockdown OCM1 and CRMM1 cells with or without PER1 and TP53 silencing. All of the experiments were performed in triplicate, and relative cell numbers are shown as means ± SD. *p < 0.05. h In ocular melanoma cells, higher histone lactylation level induced by aerobic glycolysis promoted the transcription of YTHDF2, which recognizes the m6A modification site on the RNA of two tumor suppressor genes, PER1 and TP53, and promoted their degradation and contributes to the aggressive traits in ocular melanoma progression