FIGURE 5.

PLAGL2 serves as a promising target for selenium sulfide induced proliferation inhibition and apoptosis of HCC cells in vitro and in vivo. (A) Protein levels of PLAGL2 in SK‐Hep‐1 and SMMC‐7721 cells exposed to SeS₂ (20 μM) for different durations. (B) Protein expression of PLAGL2 in SK‐Hep‐1 and SMMC‐7721 cells treated with SeS₂ for 48 h. (C) Representative images of the immunohistochemical analysis of PLAGL2 expression in SMMC‐7721 xenograft samples. The scale bar represents 50 μm. (D) Effects of SeS₂ on the proliferation of Ctrl/SK‐Hep‐1 and shPLAGL2/SK‐Hep‐1 cells. (E) Effects of SeS₂ on the proliferation of Ctrl/Bel‐7402 and PLAGL2/Bel‐7402 cells. (F) Effects of SeS₂ on the apoptosis of Ctrl/SK‐Hep‐1, shPLAGL2/SK‐Hep‐1, Ctrl/Bel‐7402, and PLAGL2/Bel‐7402 cells. (G) Effects of SeS₂ on the Δψm of Ctrl/SK‐Hep‐1 and shPLAGL2/SK‐Hep‐1 cells. (H) Effects of SeS₂ on the Δψm of Ctrl/Bel‐7402 and PLAGL2/Bel‐7402 cells. (I) Quantification histogram of (G) and (H) based on TMRE fluorescence intensity (fold change of control). (J) Images of tumors excised from four nude mice at 14 days after intraperitoneal injection of saline solution or SeS₂ (5 mg/kg) in Ctrl/Bel‐7402 and PLAGL2/Bel‐7402 xenograft tumors. (K) Tumor volume changes in the mice were measured every day. (L) Effects of SeS₂ on the masses of Ctrl/Bel‐7402 and PLAGL2/Bel‐7402 xenograft tumors. Data are expressed as the means ± SEM (n = 4). *p < 0.05, **p < 0.01 compared with the control group