Figure 7.

The excessive cancer upregulated drug-resistant (CUDR) oncogenic action was abrogated by the knockdown of highly upregulated in liver cancer (HULC) or β-catenin in the derived hepatocyte-like cells. (a) Reverse-transcription polymerase chain reaction (RT-PCR) analysis for CUDR and HULC, and western blotting analysis for β-catenin in derived hepatocyte-like cells with CUDR overexpression, CUDR overexpression plus HULC knockdown, or CUDR overexpression plus β-catenin knockdown. Loading based on β-actin. (b) Cells proliferation assay in vitro. Data are means of values from three independent experiments, bar ± standard error of the mean (SEM). **P < 0.01 or *P < 0.05. (c) Soft-agar colony-formation efficiency assay. Data are means of values from three independent experiments, bar ± SEM. **P < 0.01. (d) BrdU staining analysis. Data are means of values from three independent experiments, bar ± SEM. **P < 0.01. (e) Wound test analysis at 0 and 24 hours, respectively. Data are presented as mean ± SEM, **P < 0.01. (f) Tumorigenesis test in vivo. (A) Mice were stratified and the tumors were recovered. The photography of xenograft tumor in the four groups (indicated in left). (B) The wet weight of each xenograft tumor was determined for each mouse (n = 6). Each value was presented as mean ± standard error of the mean (SEM). **P < 0.01 shows a positive difference. (C) A portion of each tumor was fixed in 4% paraformaldehyde, embedded in paraffin and micrometers of sections (4 µm) for histological hematoxylin-eosin (HE) staining (original magnification ×100).