Fig. 3
From: Glucose-sensitive acetylation of Seryl tRNA synthetase regulates lipid synthesis in breast cancer
Acetylation of SerRS at Lys323 is essential for its tumor suppressor activity. a Western blot analysis of subcellular localization of SerRS and SIRT2 in MDA-MB-231 cells transfected with V5-tagged SIRT2 and Flag-tagged wild type (WT) or mutant SerRS, i.e., SerRSK323R or SerRSK323Q (left panel) and the coimmunoprecipitation assay using the whole cell lysates (right panel). b Chromatin immunoprecipitation assay in the lysates of MDA-MB-231 cells transfected with wild type SerRS (WT) or SerRS with K232Q mutation (means ± SEM from three independent experiments, **P < 0.01, by unpaired Student’s t-test). c Kaplan–Meier survival curve of 115 breast cancer patients with high and low SerRS protein levels. d Kaplan–Meier survival curves of indicated intrinsic subtypes of breast cancer patients with high and low SerRS mRNA levels. e The proliferation curves of MDA-MB-231 cells transfected with empty vector (Vector), WT SerRS, or mutant SerRS, i.e., SerRSK323R and SerRSK323Q. Data are plotted as means ± SEM from three independent experiments (*P < 0.05, **P < 0.01, ***P < 0.001, by two-way ANOVA). f The growth curves of tumor xenografts formed by MDA-MB-231 cells stably transfected with empty vector (Vector), wild type SerRS (SerRSWT), or SerRSK323R mutant (means ± SEM, n = 6, ***P < 0.001, by two-way ANOVA). g The growth curves of tumor homografts formed by 4T1 cells stably transfected with empty vector (Vector) or SerRS (means ± SEM, n = 7, ***P < 0.001, by two-way ANOVA,)
