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. 2013 Mar 21;19(11):1718–1727. doi: 10.3748/wjg.v19.i11.1718

Figure 4.

Figure 4

Reactivation of ubiquitin carboxyl-terminal esterase L1 by 5-AZA-2’-deoxycytidine and/or Trichostatin A treatment in pancreatic and biliary cancer cell lines. A: PK-1 cells; B: PK45P cells; C: TGBC1TKB cells. To examine the roles of CpG methylation and histone deacetylation in the silencing of ubiquitin carboxyl-terminal esterase L1, cancer cells were treated with 2 or 5 μmol/L 5-AZA-2’-deoxycytidine (5-AZA-dC) for 72 h or 100 nmol/L Trichostatin A (TSA) for 24 h. The cells were also treated with 2 μmol/L 5-AZA-dC for 72 h, followed by 100 nmol/L TSA for an additional 24 h.