Fig. 4: S100P degrades ACC1 via lysosome–dependent manner.

a Lipid metabolomics analysis in HuH7 WT and S100P KO cells, indicating that S100P inhibits the content of PUFAs. b Phosphatidylethanolamines (PE) contents in HuH7 WT and S100P KO cells. c Western blot analysis of genes about lipid synthesis or uptake in HuH7 WT and S100P KO cells. d Western blot analysis of genes about lipid synthesis or uptake in HepG2 cells expressing sg-ctrl or sg-S100P. e Western blot analysis of genes about lipid synthesis or uptake in SNU387 cells and S100P OE cells. f Western blot analysis of genes about lipid synthesis or uptake in HT1080 cells and S100P OE cells. g Western blot analysis in HuH7 cells treated with RSL3 (1 µM) for indicated times. h Western blot analysis in HuH7 cells treated with erastin (5 µM) for indicated times. i Western blot analysis in HEK293T cells transfected with indicated doses of S100P for detection of ACC1 expression. j Western blot analysis in HEK293T cells transfected with S100P for detection of ACC1 after the treatment with CHX. k Quantitative data of band gray density of ACC1 are shown. l Western blot analysis in SNU387 S100P OE cells treated with Chloroquine (CQ) and MG132, showing that CQ rather than MG132 can rescue the down-regulation of S100P to ACC1. m Western blot analysis in SNU387 S100P OE cells with the treatment of Bailomycin A1. The Western blot experiments were repeated three times independently with similar results in c–j and l, m. Data and error bars are mean ± s.d., n =  4 (S100P KO group) and n = 3 (WT group) biological independent experiments in b. n =  3 biological independent experiments in k. Statistical analysis was done with two-tailed Student’s t test. Source data are provided as a Source Data file.