Fig. 5: RAD51B deletion leads to reduced phosphorylation of EZH2 at Thr311 through AMPK pathway.
From: RAD51B-EZH2 axis as a potential therapeutic target for TNBC through cell fate conversion
A Western blot showing the expression of the indicated protein after dox-inducing Rad51b knockout in HP5008 and 545 cells. B Western blot showing the expression of the indicated protein after cells were treated with antimycin A at different concentrations. C The mRNA expression of PRC2 downstream genes in HP5008 and 545 cells with or without antimycin A treatment. Data are presented as the means ± SEM with statistical significance among groups determined by a two-tailed Student’s t test. D Cellular ATP levels in HP5008 and 545 cells with or without dox-induced Rad51b knockout. E Cellular ADP/ATP ratios in HP5008 and 545 cells with or without dox-induced Rad51b knockout. D, E Data are presented as the means ± SEM of three independent experiments, with statistical significance among groups determined by a two-tailed Student’s t test. F Western blotting showing the expression of the indicated protein after dox-inducing Rad51b knockout in MCF-7 cells. G Western blotting showing the expression of the indicated protein after MCF-7-TLCV2-sgRad51b cells treated with antimycin A in different concentrations. H The mRNA expression of PRC2 downstream genes in MCF-7-TLCV2-sgRad51b cells with or without antimycin A treatment. Data are presented as the means ± SEM with statistical significance among groups determined by a two-tailed Student’s t test.
