Fig. 6: ENO1 is a key mediator of UCHL3-regulated AKT/CCND1 signaling to promote GC progression and shows positive correlation with UCHL3 expression. | Cell Death & Disease

Fig. 6: ENO1 is a key mediator of UCHL3-regulated AKT/CCND1 signaling to promote GC progression and shows positive correlation with UCHL3 expression.

From: UCHL3 depletion inhibits gastric cancer progression and enhances palbociclib sensitivity by regulating the AKT/CCND1 signaling axis via ENO1 ubiquitination

Fig. 6: ENO1 is a key mediator of UCHL3-regulated AKT/CCND1 signaling to promote GC progression and shows positive correlation with UCHL3 expression.

A Western blot analysis of ENO1, AKT, p-AKT(s473), and CCND1 expression in MKN-28 cells transfected with UCHL3 overexpression plasmid and/or ENO1 siRNA as indicated. B–E Assessment of GC cell proliferation, invasion, and migration following transfection with UCHL3 overexpression plasmid and/or ENO1 siRNA using CCK-8 assay (B), colony formation assay (C), Transwell invasion assay (D), and wound healing assay (E). All experiments were repeated at least three times. F Representative IHC images of UCHL3 and ENO1 in two cases of GC patients. G Correlation between UCHL3 and ENO1 expression in GC tissues was analyzed by chi-square test. H Survival analysis of the 127 GC patients based on IHC scores of UCHL3 and ENO1. One-way ANOVA: *P < 0.05, **P < 0.01, ***P < 0.001.

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