【Abstract】ObjectiveTo investigate the inhibitory effects and the mechanisms of octreotide (OCT) on the growth of hepatocellular carcinoma (HCC).
MethodsBel7402 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.
ResultsWith 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 (P＜0.05). The ratio of G0/G1 cells increased markedly (P＜0.05). The proportion of Bel7402 cells expressing cMet was reduced significantly (P＜0.05). The growth of implanted tumor was inhibited with OCT treatment (P＜0.05). 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.
ConclusionOCT inhibits the growth of HCC by downregulation of cMet.
Citation：
HUA Yunpeng,LAI Jiaming,LIANG Lijian,HUANG Jiefu.. Octreotide Inhibits the Growth of Hepatocellular Carcinoma Through Down-Regulation of cMet. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2006, 13(2): 158-162. doi:
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- 1. Kouroumalis E, Skordilis P, Thermos K, et al. Treatment of hepatocellular carcinoma with octreotide: a randomised controlled study [Ｊ]. Gut, 1998; 42(3)∶442.
- 2. Kumar M, Liu ZR, Thapa L, et al. Antiangiogenic effect of somatostatin receptor subtype 2 on pancreatic cancer cell line: Inhibition of vascular endothelial growth factor and matrix metalloproteinase2 expression in vitro [Ｊ]. World J Gastroenterol, 2004; 10(3)∶393.
- 3. Casini Raggi C, Calabro A, Renzi D, et al. Quantitative evaluation of somatostatin receptor subtype 2 expression in sporadic colorectal tumor and in the corresponding normal mucosa [Ｊ]. Clin Cancer Res, 2002; 8(2)∶419.
- 4. Xie Q, Liu KD, Hu MY, et al. SF/HGFcMet autocrine and paracrine promote metastasis of hepatocellular carcinoma [Ｊ]. World J Gastroenterol, 2001; 7(6)∶816.
- 5. 申洪. 免疫组织化学染色定量方法研究（Ⅲ） [Ｊ]. 中国组织化学与细胞化学杂志, 1995; 4(1)∶89.
- 6. Tavian D, De Petro G, Benetti A, et al. uPA and cMET mRNA expression is coordinately enhanced while hepatocyte growth factor mRNA is downregulated in human hepatocellular carcinoma [Ｊ]. Int J Cancer, 2000; 87(5)∶644.
- 7. Boros P, Miller CM. Hepatocyte growth factor: a multifunctional cytokine [Ｊ]. Lancet, 1995; 345(8945)∶293.
- 8. To CT, Tsao MS. The roles of hepatocyte growth factor/scatter factor and met receptor in human cancers (Review) [Ｊ]. Oncol Rep, 1998; 5(5)∶1013.
- 9. Ueki T, Fujimoto J, Suzuki T, et al. Expression of hepatocyte growth factor and its receptor, the cmet protooncogene, in hepatocellular carcinoma [Ｊ]. Hepatology, 1997; 25(3)∶619.
- 10. Wang R, Ferrell LD, Faouzi S, et al. Activation of the Met receptor by cell attachment induces and sustains hepatocellular carcinomas in transgenic mice [Ｊ]. J Cell Biol, 2001; 153(5)∶1023.
