Research Paper Advance Articles

Pharmacological targeting of TNS3 with histone deacetylase inhibitor as a therapeutic strategy in esophageal squamous cell carcinoma

LMK-235 inhibits ESCC cells proliferation. (A) Growth curves of the five ESCC cell lines treated with LMK-235 for 48 hr. Absorbance at OD450 nm are normalized to vehicle control (0.1% DMSO; n = 5 wells/dose point). IC50 of KYSE150 is marked as the red point. (B) EdU incorporation assay of KYSE150 treated with LMK-235 (0.824 μM) for 48 hr. Scale bar = 50 μm. (C) The expressions of H3K27ac, H3K14ac, H3K9ac, HDAC4, and HDAC5 are determined by western blot in KYSE150 treated as (B). Histone H3 is used as the loading control. (D, E). Cell cycle distribution (D) and the percentage of Annexin V+ cells (E) of KYSE150 treated as (B), analyzed by flow cytometry. (A–E) Error bar denotes SEM of three replicates.

Figure 1. LMK-235 inhibits ESCC cells proliferation. (A) Growth curves of the five ESCC cell lines treated with LMK-235 for 48 hr. Absorbance at OD450 nm are normalized to vehicle control (0.1% DMSO; n = 5 wells/dose point). IC50 of KYSE150 is marked as the red point. (B) EdU incorporation assay of KYSE150 treated with LMK-235 (0.824 μM) for 48 hr. Scale bar = 50 μm. (C) The expressions of H3K27ac, H3K14ac, H3K9ac, HDAC4, and HDAC5 are determined by western blot in KYSE150 treated as (B). Histone H3 is used as the loading control. (D, E). Cell cycle distribution (D) and the percentage of Annexin V+ cells (E) of KYSE150 treated as (B), analyzed by flow cytometry. (AE) Error bar denotes SEM of three replicates.