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. 2012 Jul 30;32(27):3286–3295. doi: 10.1038/onc.2012.334

Figure 2.

Figure 2

Knockdown of mutant p53 in EC cells causes a reversal of EMT and inhibition of cell invasion ability. (a) Morphology of endometrial cancer HEC-1 cells transfected with control shRNA vector or p53 shRNA vector (scale bar=100 μm). (b) Protein levels of p53 and EMT markers as analyzed by western blot. (c) Invasion of HEC-1 cells after p53 shRNA transfection (mean±s.d.; n=3; *P<0.01). Representative images of invaded cells are shown. (d) Images show mammosphere formation in HEC-1 cells after p53 silencing by shRNA. Number of spheres obtained from 1000 cells at 12 days after plating (scale bar=50 μm; mean±s.d.; n=3; *P<0.01). (e) Control- or p53 shRNA-transfected HEC-1 cells were treated with paclitaxel (0, 15, and 30 nmol/l) for 48 h. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (mean±s.d.; n=3; *P<0.01). (f) Relative mRNA expression of stemness markers (normalized to GAPDH) in HEC-1 cells after p53 silencing, determined by qRT–PCR (mean±s.d.; n=4; *P<0.01).

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