Fig. 6

ACSL1 expression in MCF7/TAM cells is regulated by CSE through protein interactions and sulfhydrylation modification of PPARγ. (A and B) Expression levels of PPARγ in ER+ breast cancer TAM-resistant cells MCF7/TAM. All data are expressed as mean ± standard deviation (n = 3). *P < 0.05, ***P < 0.001 versus MCF7 cells. (C and D) Effect of down-regulation of CSE on PPARγ expression in MCF7/TAM cells. All data are expressed as mean ± standard deviation (n = 3). *P < 0.05 versus Sc siRNA group. (E) CSE interaction with PPARγ. The overexpression plasmids of CSE and PPARγ were cotransfected into MCF7/TAM cells, followed by co-immunoprecipitation assay. (F) Effect of down-regulation of CSE on PPARγ binding to the ACSL1 promoter in MCF7/TAM cells. Overexpression plasmids of ACSL1 promoter and PPARγ were cotransfected into MCF7/TAM cells, which were then assayed by applying a dual luciferase reporter gene assay kit. All data are expressed as mean ± standard deviation (n = 3). **P < 0.01 versus ACSL1 + PPARγ group. (G and H) Effect of down-regulation of CSE protein on PPARγ sulfhydrylation levels in MCF7/TAM cells. The maleimide method was applied to detect the level of PPARγ sulfhydration. All data are expressed as mean ± standard deviation (n = 3). **P < 0.01 versus Sc siRNA group.