Octreotide induces caspase activation and apoptosis in human hepatoma HepG2 cells

Figure 1 Octreotide at a concentration of 10^-8 mol/L had a statistically significant inhibitory effect on cellular proliferation of HepG2 hepatocellular carcinoma cells, compared to untreated cells. Lower concentrations caused an initial increase in proliferation. The results represent the mean of 8 different experiments ± SE (^bP < 0.01, ^dP < 0.001). NS: Not significant.

Figure 2 Tumor necrosis factor-α at concentrations of 10, 20 and 100 ng/mL had a statistically significant inhibitory effect on cellular proliferation of HepG2 cells, compared to untreated cells. The results represent the mean of 8 different experiments ± SE (^dP < 0.001). TNF-α: Tumor necrosis factor-α.

Figure 3 Detection of DNA fragmentation revealed a non significant increase in DNA fragments, after 24-h treatment with octreotide or tumor necrosis factor-α (n = 8). TNF-α: Tumor necrosis factor-α; NS: Not significant.

Figure 4 The apoptotic effect of octreotide and tumor necrosis factor-α alone is shown. A: Octreotide and tumor necrosis factor-α (TNF-α) significantly increased early (Annexin-V only positive, right lower quadrant) and more so late apoptotic cells [Annexin-V and propidium iodide (PI) positive, right upper quadrant]. Every sample was analyzed with the same gating strategy (Gate A) to exclude debris and non-specific binding of Annexin-V, while control refers to uninduced HepG2 cells; B: Annexin-V positive cells; C: Annexin-V/PI positive cells. B and C: Mean of 8 different experiments ± SE (^bP < 0.01, ^dP < 0.001).

Figure 5 Caspase-2 (A), -3 (B), -8 (C) and -9 (D) activities, after treatment of HepG2 cells with 10^-8 mol/L octreotide and 20 ng/mL tumor necrosis factor-α, compared to untreated cells. The results represent the mean of 10 different experiments ± SE (^bP < 0.01, ^dP < 0.001). TNF-α: Tumor necrosis factor-α; NS: Not significant.