AGS, NCI-N87, MGC-803, and MKN1, in which miR-375 was down-regulated, were treated with demethylating agent (5-Aza) and histone deacetylases inhibitor43 (link). For 5-Aza (Sigma, St Louis, MO) treatment group, the cells were treated with 10 μM 5-Aza for 3 days. For TSA (Sigma) treatment group, 100 nM TSA was added to the cells for 24 h. For the combination treatment, the cells were treated with 5-Aza for 4 days and in the last 24 h, 100 nM TSA was added. The control cultures were treated with an equal amount of vehicle DMSO (Sigma).
Verteporfin (also named VP, Selleckchem, Houston, TX), a small molecule inhibitor of YAP1-TEAD association which inhibits YAP1’s oncogenic property was used in MKN28, AGS, MGC-803, and SGC-7901 cells to investigate the effect of pharmacological inhibition of YAP144 (link),45 (link). The cells were treated with VP in 0, 1, 2, 5, 10 μM concentrations for a 3-day MTT assay. For the Western blot analysis of YAP1 and CTGF, the protein was collected in 0, 1, 2 μM of VP treatment for 24 h.
Verteporfin (also named VP, Selleckchem, Houston, TX), a small molecule inhibitor of YAP1-TEAD association which inhibits YAP1’s oncogenic property was used in MKN28, AGS, MGC-803, and SGC-7901 cells to investigate the effect of pharmacological inhibition of YAP144 (link),45 (link). The cells were treated with VP in 0, 1, 2, 5, 10 μM concentrations for a 3-day MTT assay. For the Western blot analysis of YAP1 and CTGF, the protein was collected in 0, 1, 2 μM of VP treatment for 24 h.
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