Figure 2.

Oncogenic potential of STC2 in HCC. (A) Cell proliferation assays. STC2 was overexpressed or knocked down in HepG2. Altered STC2 expression was confirmed by Western blotting (left panel). The cell proliferation was determined by MTT. **p<0.01 (vs control). (B) Colony formation. HepG2, HepG2/STC2 (overexpression) and HepG2/shSTC2 (knockdown) cells were seeded in 6-well plates and incubated at 37°C, 5% CO₂ for two weeks to grow discrete colonies. The number of foci containing >50 cells was counted and statistically analyzed. *p<0.05 and **p<0.01 (vs control). (C) Xenograft model. HepG2, HepG2/STC2 and HepG2/shSTC2 (2 × 10⁶ cells) were subcutaneously transplanted into the posterior flanks of mice (n=6 in each group). Tumor volume were recorded every 3 days. After 24 days, the mice were sacrificed. The tumors were collected and analyzed. **p<0.01 (vs control). (D) PCNA expression. The tumor slides were stained with anti-PCNA antibody (1:200). The positive rates of PCNA were calculated and analyzed. **p<0.01 (vs control). (E) The protein expression p-AKT, total AKT, Cyclin D1 and internal loading control GAPDH were examined by Western blotting, and the expression ratio of p-AKT/AKT and Cyclin D1 normalized GAPDH were quantified and analyzed. **p<0.01 (vs control).