The study of inhibition effect of octreotide on the growth of hepatocellular carcinoma xenografts in situ in nude mice.
- Author:
Yun-peng HUA
1
;
Jie-fu HUANG
;
Li-jian LIANG
;
Shao-qiang LI
;
Jia-ming LAI
;
Hui-zhen LIANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antineoplastic Agents, Hormonal; therapeutic use; Humans; Liver Neoplasms, Experimental; drug therapy; metabolism; pathology; Mice; Mice, Nude; Neoplasm Transplantation; Octreotide; therapeutic use; Proto-Oncogene Proteins c-met; biosynthesis; Receptors, Somatostatin; biosynthesis; Smad2 Protein; biosynthesis; Transforming Growth Factor beta; biosynthesis
- From: Chinese Journal of Surgery 2005;43(11):721-725
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of octreotide (OCT) on inhibiting hepatocellular carcinoma (HCC) and investigate its mechanisms.
METHODSNude mice bearing xenografts in situ were treated with OCT or saline control for 7 weeks since tumor implantation. The immunohistochemistry for somatostatin receptor 2 (SSTR2), cMet, transforming growth factor beta1 (TGFbeta1), phospho-Smad2, Smad4 and Smad7 was performed. SSTR2 and Smad4 mRNA expression was measured by semi-quantitative RT-PCR.
RESULTSAfter OCT treatment, the mean tumor weight in mice given OCT (0.17 +/- 0.14 g) was significantly lower than that of the control group (0.53 +/- 0.06 g). The inhibition rate of tumor was 67.9%. mRNA and protein expression of SSTR2, Smad4 in tumor cells of the treatment group were significantly more than that of the control group. cMet expression in OCT group was remarkably lower than that in control group. Between two groups, the expression of TGFbeta1, phospho-Smad2 and Smad7 were not remarkably different. In addition, phospho-Smad2 expression in HCC was significantly less than that of the normal hepatic cell.
CONCLUSIONOCT can inhibit the growth of HCC xenografts markedly. The mechanisms of OCT-induced inhibition effect may be related to up-regulating SSTR2 expression, down-regulating cMet, and recovering the function of TGFbeta/Smads-induced antitumor. In addition, the decreased expression of phospho-Smad2 may be an important feature of Bel7402 cells.
