Trichostatin A augments cell migration and epithelial-mesenchymal transition in esophageal squamous cell carcinoma through BRD4/c-Myc endoplasmic reticulum-stress pathway

Figure 5 Trichostatin A promotes epithelial-mesenchymal transition of esophageal squamous cell carcinoma cells through bromodomain-containing protein/cellular myelocytomatosis oncogene/endoplasmic reticulum-stress pathway is reversed by inhibitor of trichostatin A 1. A: Representative images of the migration of Eca109 and EC9706 cells treated with trichostatin A (TSA) combined with inhibitor of trichostatin A 1 (ITSA1) from Transwell assays; B: Western blot shows after TSA combined with ITSA1 that acetylated histones H3, acetylated histones H4, cellular myelocytomatosis oncogene, glucose-regulated protein 78 levels decreased, and epithelial-mesenchymal transition marker E-cadherin levels increased, vimentin, β-catenin levels decreased. Cell counts are for the corresponding assays of at least five random microscope fields (100 magnification). ^aP < 0.05. ^bP < 0.01. Bar is 50 μm. TSA: Trichostatin A; ITSA1: Inhibitor of trichostatin A 1; GRP78: Glucose-regulated protein 78; acH3: Acetylated histones H3; c-Myc: Cellular myelocytomatosis oncogene.