Octreotide Inhibits the Growth of Hepatocellular Carcinoma Through Down-Regulation of cMet
Huang Jie-f
Abstract
Huang Jie-f
Abstract
Objective To investigate the inhibitory effects and the mechanisms of octreotide(OCT) on the growth of hepatocellular carcinoma(HCC).Methods Bel7402 HCC cells were studied for proliferative ability by MTT assay,morphology by light microscopy,adhesive and invasive ability by cell adhesion and wound strack experiments.Immunofluorescence flow cytometry was used for study of cMet expression and cell cycle as well. Furthermore,the effects of OCT on tumor growth metastasis were investigated in nude mice with implanted HCC.The expression of cMet in implanted tumor cells was studied by immunohistochemistry.Results With OCT treatment,the proliferative ability of Bel7402 cells and cell morphology didn't change.The adhesive and invasive ability decreased compared with no OCT treatment cells(P0.05).The ratio of G_0/G_1 cells increased markedly (P0.05).The proportion of Bel7402 cells expressing cMet was reduced significantly(P0.05).The growth of implanted tumor was inhibited with OCT treatment(P0.05).The intensity of cMet expression in OCT group was remarkably weaker than that in control group.In addition,no recurrence and metastasis was found in OCT group 7 weeks after curative resection of xenografts,while 3 cases in controd group were observed to have the recurrence and metastasis.The intensity of cMet immunolabeling in the metastatic tumors was higher than that in xenografts of control group,but the difference was not significant.Conclusion OCT inhibits the growth of HCC by down-regulation of cMet.
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Objective To investigate the inhibitory effects and the mechanisms of octreotide(OCT) on the growth of hepatocellular carcinoma(HCC).Methods Bel7402 HCC cells were studied for proliferative ability by MTT assay,morphology by light microscopy,adhesive and invasive ability by cell adhesion and wound strack experiments.Immunofluorescence flow cytometry was used for study of cMet expression and cell cycle as well. Furthermore,the effects of OCT on tumor growth metastasis were investigated in nude mice with implanted HCC.The expression of cMet in implanted tumor cells was studied by immunohistochemistry.Results With OCT treatment,the proliferative ability of Bel7402 cells and cell morphology didn't change.The adhesive and invasive ability decreased compared with no OCT treatment cells(P0.05).The ratio of G_0/G_1 cells increased markedly (P0.05).The proportion of Bel7402 cells expressing cMet was reduced significantly(P0.05).The growth of implanted tumor was inhibited with OCT treatment(P0.05).The intensity of cMet expression in OCT group was remarkably weaker than that in control group.In addition,no recurrence and metastasis was found in OCT group 7 weeks after curative resection of xenografts,while 3 cases in controd group were observed to have the recurrence and metastasis.The intensity of cMet immunolabeling in the metastatic tumors was higher than that in xenografts of control group,but the difference was not significant.Conclusion OCT inhibits the growth of HCC by down-regulation of cMet.
Key concepts: Flow cytometry, Metastasis, Hepatocellular carcinoma, Immunohistochemistry, Cell growth, Octreotide, Cancer research, Cell cycle