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