Research Article

UBE2C Induces Cisplatin Resistance via ZEB1/2-Dependent Upregulation of ABCG2 and ERCC1 in NSCLC Cells

Figure 5

Knockdown of ZEB1/2 inhibits UBE2C-dependent cellular growth, invasiveness, and EMT in DDP-resistant NSCLC cells. (a) Colony formation assay demonstrating that ectopic expression of UBE2C significantly enhanced colony formation density, which was blocked by knockdown ZEB1 in A549/DDP cells with treatment of DDP at 6 μg/ml for 48 h. (b) SA-β-Gal assay was performed to detect the cell senescence of A549/DDP cells treated with DDP at 6 μg/ml for 48 h and transfected with UBE2C, siUBE2C alone, or the combination of siZEB1/2 and ZEB1/2 plasmid for 48 h. (c, d) Scratch assay (c) and Matrigel invasion assay (d) indicated that UBE2C promote cell migration and invasion via regulating ZEB1 in A549/DDP cells with treatment of DDP at 6 μg/ml for 36 h. (e, f) UBE2C significantly decreased E-cadherin and increased vimentin in mRNA (e) and protein (f) levels by regulating ZEB1/2 in the A549/DDP cells with treatment of DDP at 6 μg/ml for 48 h. Results were presented as mean ± SD, and the error bars represent the SD of three independent experiments. p<0.05; p<0.01 versus control group.
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