Fig. 6: Potential mechanisms underlying the ATO-induced inhibition of 14-3-3ε. | Cell Death Discovery

Fig. 6: Potential mechanisms underlying the ATO-induced inhibition of 14-3-3ε.

From: Arsenic trioxide enhances the chemotherapeutic efficiency of cisplatin in cholangiocarcinoma cells via inhibiting the 14-3-3ε-mediated survival mechanism

Fig. 6

a HuCCT1 and RBE cells were treated by 0.0 or 2.0 μM of ATO for 12 h, qPCR analysis in triplicate of 14-3-3ε mRNAs. b PyMol software analyses of the relationship between 14-3-3ε and14-3-3η, and the binding of ATO to this heterodimers. c, left After HuCCT1 cells were pre-treated by 20 μM of MG-132 for 2 h, they were treated by 0.0 or 2.0 μM of ATO for 6 h, Co-IP analyses of the binding of 14-3-3ε with 14-3-3η or ubiquitin. c, right The graph was a statistical analysis for the ubiquitination degree of 14-3-3ε. d HuCCT1 and RBE cells were treated by 0.0 or 2.0 μM of ATO for 24 h, Western blot (left) and quantitative analysis (right) of the expressions of 14-3-3ε and 14-3-3η. **p < 0.01 vs. control group.

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