ABSTRACT
Objective To investigate the effect and mechanism of oetreotide (OCT) on DENA related hepatoeareinogenesis in rats. Methods Fresh diethylnitrosamine (DENA) solution was given to induce the model of rat hepatoeellular carcinoma. The rats were divided randomly into two groups: OCT treatment group and control group. The survival rate and hepatoeareinogenesis rate were observed. SSTR2 mRNA and protein expression were measured. Results The survival rote of OCT treatment group (70.0%, 7/10) was significantly higher than that of control group (30.0%, 6/20) (X2 = 4.344, P<0.05). 16 weeks after DENA treatment, the difference of bepatoearcinogenesis rate between the two groups was not remarkable though the value of OCT treatment group (0%, 0/10) was lower than that of control groups (30.0%, 6/20)(X2 = 3.750, P＞0.05). However, 22 weeks after DENA treatment, hepatoeareinogenesis in control group (83.3%, 10/12) was markedly higher than that in OCT treatment group (22.2% , 2/9)(X2 =7.843, P<0.01). With liver cirrhosis progressing, the expressions of SSTR2 mRNA and protein increased, and reached the peak 16 weeks after DENA treatment, then began to decrease. The expressions of SSTR2 mRNA and protein in hepatocellular carcinoma were significantly lower than those in the liver 22 weeks after DENA treatment (F = 35.010 and 13. 386, P<0.01). The expression levels in OCT treatment group were similar to those in control group 8 and 16 weeks after DENA treatment. But the expression levels in OCT group 22 weeks after DENA treatment didn't lower markedly, and were higher significantly than those in control group (t = 2.806 and 4.498, P<0.05). Conclusion OCT can inhibit efficiently hepatocareinogenesis and reduce the mortality of rots treated with DENA possibly by a mechanism maintaining the expression levels of SSTR2.
ABSTRACT
Objective To investigate the anti-migratory and anti-invasive effect of somatostatin receptor type 2(SSTR2) gene transfection mediated by adenovirus in human pancreatic carcinoma cell and the mechanisms involved in this effect.Methods The full length human SSTR2 cDNA was introduced into pancreatic cancer cell line BXPC-3 by adenovirus-mediated transfection,and stable expression of RNA and protein of SSTR2 were detected by RT-PCR and Westen-blot.The Matrigel coated Transwell was used to detect the migratory and invasive ability of SSTR2expressing cells,Adv-GFP control cells and mock control cells.Furthermore,the expressions of matrix metalloproteinase-2(MMP-2) and tissue inhibitor of metalloproteinase-2(TIMP-2) were detected by RT-PCR method in these cells.Results The stable expression of SSTR2 was detected in BXPC-3 cells transfected by Adv-GFP-SSTR2.A dramatic decrease of BXPC-3 expressing SSTR2 cell(migrated) through a Matrigel-coated filter was observed,as compared with Adv-GFP control cells and mock control cells(P
ABSTRACT
Objective To investigate the mRNA and protein expression of somatostatin receptors in hepatocellular carcinoma HCCLM3 cell lines and to explore the mechanism by which somatostatin effects on hepatocellular carcinoma. Methods RT-PCR., immunocytochemistry and MTT were used to detect mRNA and protein expression of somatostatin receptors in hepatocellular carcinoma cells and evaluate the antiproliferative effect of somatostatin. Results The effect of somatostatin on the cellular proliferation was verified. Immunocytochemistry study revealed a mainly intracellular distribution of all SSTRs with unique patterns for each of them. mRNA expression of all 5 subtypes of somatostatin receptors was different, SSTR2 and SSTR1 mRNA expressions were significantly higher than SSTR3, SSTR4 and SSTR5 ( P