YDJC Induces Epithelial-Mesenchymal Transition via Escaping from Interaction with CDC16 through Ubiquitination of PP2A

Figure 3

The deacetylase activity of YDJC promotes EMT of lung cancer cells. (a) YDJC siRNA suppresses and YDJC overexpression promotes SPC-induced EMT in A549 lung cancer cells. (b) YDJC siRNA suppressed SPC-induced EMT, and YDJC overexpression promoted EMT in H838 and H1299 lung cancer cells. (c) Confocal microscopic analysis of EMT markers and YDJC in SPC-induced EMT of A549 lung cancer cells. (d) YDJC siRNA suppressed and YDJC overexpression promoted SPC-evoked migration and invasion in A549, H838, and H1299 lung cancer cells. (e) TGF-β1 was unable to induce changes of EMT markers such as E-cadherin and N-cadherin in YDJC stably knockdown A549 lung cancer cells (). In (a)-(d), the YDJC gene was silenced by transfecting the A549, H838, and H23 cells with the YDJC siRNA or control siRNA followed by stimulation with or without 5 μM SPC for 48 h. (f) Effects of YDJC deacetylase activity on SPC-induced E-cadherin and N-cadherin expression. The overexpression of plasmids containing YDJC and (a dominant negative form of deacetylase) cDNA were analyzed by transfecting A549 cells with the plasmid containing YDJC or and a control empty vector (4 μg) followed by treatment with SPC (5 μM) for 48 h. (g) Confocal microscopic analysis of the effects of the deacetylase activity of YDJC on SPC-induced E-cadherin and N-cadherin expression. Effects of the deacetylase activity of YDJC on SPC-promoted migration and invasion. In (e) and (f), cell lysates were analyzed by Western blotting. YDJC gene overexpression was analyzed by transfecting A549, H838, and H1299 cells with a plasmid having YDJC or an empty vector (4 μg) and subsequent treatment with SPC (5 μM) for 48 h.