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Objective: To figure out the effect of somatostatin analogue Octreotide on proliferation and invasion of human hepatocellular carcinoma cell MHCC97-H and the underlying mechanism in vitro and in vivo. Methods: MHCC97-H cells were treated with Octreotide at the concentration of 0.2 ug/mL in vitro, proliferation related to time was evaluated. After treated with Octreotide at the concentration of 0.2 ug/mL for 48 h, MHCC97-H cells were observed by transmission electron microscope. Cell proliferation was detected by MTT assay after MHCC97-H cells were treated with Octreotide at different concentrations including 0.05, 0.1, 0.2, 0.4, 0.6 and 0.8 ug/mL for 36 h in vitro. 27 nude mice, in which MHCC97-H tumor mass was planted orthotopically, were divided into 3 groups randomly including control group (intraperitoneal injection with equal volume normal saline; n=8), low dose treated group (intraperitoneal injection with Octreotide at 50 ug/kg?d; n=9) and large dose treated group (intraperitoneal injection with Octreotide at 200 ug/kg?d; n=10). All mice were raised for 35 d and sacrificed. The information about survival time, the weight at death point and the pathology change of liver and lung was collected. The expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinases-2 (MMP-2) in mouse HCC tissues were detected by immunohistochemistry finally. Results: MTT assays showed that Octreotide inhibited the proliferation of MHCC97-H cells significantly. Apoptosis cells were found by transmission electron microscope after treatment with Octreotide at 0.2 ug/mL for 48 h in vitro. The proliferation was inhibited significantly by Octreotide in a dose-dependant manner (r=0.86, P<0.01). Compared with control group, the treated group had the heavier weight at death point and lower intrahepatic metastasis ratio (P<0.05), meanwhile, there was not significant difference in treated groups (P>0.05). The positive expression ratios of VEGF and MMP-2 in treated groups were lower than those in control group (P<0.05), while there was no apparent difference in treated groups (P>0.05). Conclusion: Octreotide could inhibit the proliferation of MHCC97-H cells in vitro via inducing apoptosis and the inhibitory function acts in a dose-dependant manner. Octreotide could improve survival of mice with MHCC97-H cells and inhibit the metastasis of MHCC97-H cells in vivo. Regulation of VEGF and MMP-2 expression by Octreotide would be involved in its inhibition in vivo.
Objective: To figure out the effect of somatostatin analogue Octreotide on proliferation and invasion of human hepatocellular carcinoma cells MHCC97-H and the underlying mechanism in vitro and in vivo. Methods: MHCC97-H cells were treated with Octreotide at the concentration of 0.2 μg / mL in vitro, proliferation related to time was evaluated. After treated with Octreotide at the concentration of 0.2 ug / mL for 48 h, MHCC97-H cells were observed by transmission electron microscope. Cell proliferation was detected by MTT assay after MHCC97-H cells were treated with Octreotide at different intensities including 0.05, 0.1, 0.2, 0.4, 0.6 and 0.8 ug / mL for 36 h in vitro. 27 nude mice, in which MHCC97-H tumor mass was planted orthotopically, were divided into 3 groups randomly including control group (intraperitoneal injection with equal volume normal saline; n = 8), low dose treated group (intraperitoneal injection with Octreotide at 50 μg / kg? d; n = 9) and large dose treated group al injection with Octreotide at 200 μg / kg • d; n = 10). All mice were raised for 35 d and sacrificed. The information about survival time, the weight at death point and the pathology change of liver and lung was collected. The Expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinases-2 (MMP-2) in mouse HCC tissues were detected by immunohistochemistry finally. Results: MTT assays showed that Octreotide inhibited the proliferation of MHCC97-H cells significantly. Apoptosis cells were found by transmission electron microscope after treatment with Octreotide at 0.2 ug / mL for 48 h in vitro. The proliferation was marked by Octreotide in a dose-dependent manner (r = 0.86, P <0.01). Compared with control group, the treated group had the heavier weight at death point and lower intrahepatic metastasis ratio (P <0.05), while there was no significant difference in treated groups (P> 0.05). The positive expression ratios of VEGF and MMP-2 in treated groupswere lower than those in control group (P <0.05), while there was no apparent difference in treated groups (P> 0.05). Conclusion: Octreotide could inhibit the proliferation of MHCC97-H cells in vitro via inducing apoptosis and the inhibitory function acts in a dose-dependent manner. Octreotide could improve survival of mice with MHCC97-H cells and inhibit the metastasis of MHCC97-H cells in vivo. Regulation of VEGF and MMP-2 expression by Octreotide would be involved in its inhibition in vivo.