Abstract:
Objective:To study the regulatory effect of somatostatin analogue octreotide on human gastric cancer cell line SGC7901 and to explore the corresponding mechanisms. Methods:Moderately differentiated human gastric carcinoma SGC-7901 cells were treated with octreotide in vitro. SGC- 7901 cells treated with5-FU were the positve controls and human fibroblasts were the normal controls. MTT assay was used to ob -serve the inhibitory effect of octreotide on human gastric carcinoma cells and human fibroblasts. We observed the apoptosis through fluorescent microscope. The influence of octreotide on cell cycle distribution and the apoptosis rate of human gastric carcinoma cell were analyzed with FCM. Radiommunoassay was employed to determine the changes in IGF-1 levels in cell culture fluid. Results: Octretide can not inhibit the growth of gastric cells at low concentration (50ug/L). With the increase of octretide concentration, the inhibitory effect in-creased gradually, in a dose-dependent manner. Octretide had an evident inhibitory effect on human fibro -blasts (P>0.05). There was no difference in the inhibition of SGC- 7901 cell growth between octretide ( 500 ug/ L) and 5-FU (50mg/L) (P>0.05). At 48hours after treatment with octretide (1mg/L), the morphological changes of apoptosis were seen under fluorescent microscope. At48hours after treatment with octretide ( 500 ug/L), most cells were blocked at G 0/G1 phase (72.07± 2.40). The percentage of cells at S phase was decreased sig-nificantly ( 14.99± 1.42). The proliferation of cells was inhibited and the apoptosis rate was increased (21.40±2.71). With octretide treatment at different concentrations, IGF-1 level in cell culture fluid was significantly low -er than that in the control group (P<0.01), indicating that octretide down-regulated IGF- 1 level in the cell cul -ture system. Conclusion:Octroetide can inhibit the growth of gastric carcinoma cells in vitro, with no significant inhibition on the growth of non-target cells. Octroetide can induce gastric cancer cell stagnation at G0/G1 phase and apoptosis, inhibiting the proliferation directly. Octroetide can also inhibit the secretion of IGF and restrain tumor cell growth indirectly.