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Fig. 6 | Journal of Translational Medicine

Fig. 6

From: ESRRG-PKM2 axis reprograms metabolism to suppress esophageal squamous carcinoma progression and enhance anti-PD-1 therapy efficacy

Fig. 6

Therapeutic efficacy of the DY131 ESRRG agonist in ESCC. A ESCC cells were treated with various concentrations of DY131 for 24 h. Cell viability was determined by the CCK-8 assay. The IC50 value of DY131 in ESCC cell lines was then determined. B–E Efficacy of DY131 on colony formation (B, C) and DNA synthesis (D, E) of ESCC cells (n = 3). F Effects of DY131 on extracellular acid ratio (ECAR) in TE1 cell (n = 3). G Two different RCC organoids treated with DY131, the diameters kof organoids in two groups were compared. (n = 10). H–K ECa109 and KYSE510 cells were knocked down for ESRRG and further silenced for PKM, followed by determination of ATP production (E), glucose consumption (F), pyruvate production (G) and lactate production (H) (n = 3). L After TE1 cell implantation, DY131 or vehicle was intraperitoneally injected into mice every other day and the tumor volume were monitored at indicated time points. G The weight of tumours was measured at time of sacrificed (n = 4). N Immunohistochemical analysis of mouse samples. Values are presented as mean ± SD. *P < 0.05 or **P < 0.01 indicates significant differences from the vehicle group as assessed by a one-way ANOVA with a post hoc Dunnett’s test

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