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. 2017 Sep 26;14(6):6869–6875. doi: 10.3892/ol.2017.7060

Figure 3.

Figure 3.

HDAC1 contributed to chidamide resistance in the A549 lung cancer cell line. (A) HDAC1 expression in A549 cells transfected with empty vector controls or a HDAC1 plasmid. (B) HDAC activity in A549 cells with or without HDAC1 overexpression. (C) Relative viability of HDAC1-overexpressing and parental A549 cells following treatment with 5 µM chidamide for 72 h. The (D) protein level of HDAC1, (E) relative HDAC activity and (F) relative viability following treatment with 50 µM chidamide for 72 h in A549-CHI-R and HDAC1-KO A549-CHI-R cells. *P<0.01 vs. control; **P<0.005 vs. control or A549 cells. All experiments were performed three times. HDAC, histone deacetylase; KO, knockout; Ctrl, control; A549-CHI-R, chidamide-resistant A549 cells.