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

Figure 5.

Figure 5

Histone lactylation enhances tumor proliferation and migration largely dependent on PDGFRβ pathway. (A) Representative flow cytometry histogram of PDGFRβ in ccRCC cells with or without PDGFRβ overexpression. Cells were treated with 8mM oxamate for 24 h. Overexpressing PDGFRβ restored the oxamate-induced down-regulation of PDGFRβ. (B) Quantification of relative PDGFRβ MFI in 786-O (left panel) and A498 (right panel) cells with or without PDGFRβ overexpression treated with oxamate. (C, D) CCK-8 assay showing the proliferation ability of 786-O (C) and A498 (D) cells with or without PDGFRβ overexpression treated with oxamate. (E) Transwell assay showing the migration ability of 786-O and A498 cells with or without PDGFRβ overexpression treated with oxamate. (F) Quantification of relative PDGFRβ MFI in Caki-1 cells with or without PDGFRβ knockdown. Cells were treated with 5mM lactate for 24 h. PDGFRβ knockdown inhibited the lactate-induced up-regulation of PDGFRβ. (G) CCK-8 assay showing the proliferation ability of Caki-1 cells with or without PDGFRβ knockdown treated with lactate. (H) Transwell assay showing the migration ability of Caki-1 cells with or without PDGFRβ knockdown treated with lactate. Data are presented as mean ± SD. **p<0.01, ***p<0.001, by 1-way ANOVA (B, C, D, E, F, G, H). oe, overexpression.