Fig. 4: Endogenous lactate-induced histone lactylation increases CXCL16 expression of CAFs. | Experimental & Molecular Medicine

Fig. 4: Endogenous lactate-induced histone lactylation increases CXCL16 expression of CAFs.

From: H3K18 lactylation in cancer-associated fibroblasts drives malignant pleural effusion progression via TNFR2+ Treg recruitment

Fig. 4

a Western blot analysis of the indicated proteins in CAFs treated with increasing concentrations of exogenous lactate or glucose for 48 h. b CXCL16 concentrations in CAFs supernatant after exogenous lactate treatment. c, d Lactate (c) and CXCL16 (d) levels in CAFs supernatant after treatment with glucose for 48 h. e Western blot analysis of the indicated proteins in CAFs treated with DCA, oxamate or rotenone for 48 h. f Schematic of LDHA knockdown in CAFs. g Lactate in the culture supernatant of LDHA-knockdown CAFs. h Western blot analysis of the indicated proteins in LDHA-knockdown CAFs. i CXCL16 levels in the supernatant of LDHA-knockdown CAFs. j Western blot analysis of the indicated proteins in CAFs treated with increasing concentrations of β-alanine, lactylation modulator, for 48 h. k CXCL16 concentrations in CAFs supernatant after β-alanine treatment. Data shown in ae and gk are representative of at least three independent experiments (mean ± s.d.). Statistical analysis was performed using one-way ANOVA (bd, g, i and k). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. ns not significant, KD knockdown, sh-LDHA shRNA against LDHA, sh-NC negative control.

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