Skip to main content

Advertisement

Fig. 1 | BMC Cancer

Fig. 1

From: The histone deacetylase inhibitor trichostatin a decreases lymphangiogenesis by inducing apoptosis and cell cycle arrest via p21-dependent pathways

Fig. 1

Effects of HDACi on primary human lymphatic endothelial cells. a, b Cells were exposed to increasing concentrations of trichostatin A (TSA), sodium butyrate (NaB) and valproic acid (VPA) alone and (c) in the presence or absence of 20 ng/ml VEGF-A and 100 ng/ml VEGF-C for 24 h as indicated. Cell proliferation and viability was measured using the BrdU (a, c) and Alamar blue assay (b). Average absorbance values (mean ± SE) from 4 wells per experimental condition are displayed; data are expressed as cell proliferation and vialibity in percentage (%) with regard to solvent controls (=100%; ethanol and H2O). Results were confirmed in four independent sets of experiments. *p < 0.05 vs Ctrl. d Quantification of cytotoxicity. Cells were incubated with increasing concentrations of TSA for 24 h as indicated. Cytotoxicity was quantified by using the LDH assay. Average absorbance values (mean ± SE) from quadruplicate determinations per experimental condition were calculated; data are expressed as cytotoxicity in percentage (%). e A two-dimensional, short term in vitro Matrigel assay of LECs that were left untreated or were incubated with 400 nM TSA for 6 h on Matrigel. Results were confirmed in three independent sets of experiments

Back to article page