Fig. 4
From: Targeting the CoREST complex with dual histone deacetylase and demethylase inhibitors
Pharmacologic effects of corin and related compounds on melanoma cells and the role of CoREST. a Western blot depicting increases in histone H3K4 methylation and H3K9 acetylation in WM983B melanoma cells induced by 10 µM inhibitor treatment. b Corin (EC50 = 0.095 ± 0.017 µM) was more potent than MS-275 (EC50 = 0.42 ± 0.07 µM) and more efficacious at inducing histone H3K9 acetylation in WM983B melanoma cells as determined by ELISA after 24 h treatment (n = 3). c Treatment with corin (1 µM) for 72 h potently inhibited cell growth across a panel of ten melanoma cell lines without significantly affecting primary melanocytes whereas MS-275 (1 µM) was similarly potent toward transformed and non-transformed cells (n = 3). d Knockdown of CoREST1 inhibits WM983B melanoma cell proliferation (n = 3). e, f Knockdown of CoREST1 enhances the potency of MS-275 but does not affect the potency of corin as determined after 72 h treatment (n = 3). g, h Knockdown of SIN3A inhibits WM983B melanoma cell proliferation but does not sensitize cells to the antiproliferative effects of MS-275 after 72 h treatment (n = 3). Note that cell proliferation was determined using the PicoGreen® cell proliferation assay and data were normalized to zero inhibitor concentration for individual cell lines (scrambled shRNA and CoREST shRNA1). Data (mean ± SEM) are representative of at least two independent experiments (unpaired t test, *p < 0.05, **p < 0.01, ***p < 0.001)
