ObjectiveTo detect the expression of somatostatin receptor Ⅱ(SSTR2) mRNA in the specimens of colorectal cancer patients and discuss the relationship between the expression and characteristics of the tumor.MethodsAll tissue samples of 36 cases, including normal colonic mucosa (10 cm beyond the tumor), mucosa adjacent to the tumor (within 2 cm of the tumor), tumor, and mesenteric lymph node, were collected immediately after surgical resection. The SSTR2 mRNA were detected by RT-PCR in 135 samples of the 36 cases. The SSTR2 mRNA expression rate in different samples was compared.ResultsThe SSTR2 mRNA expression rate of normal colonic mucosa, mucosa adjacent to tumor, tumor, mesenteric node without metastasis, and mesenteric node with metastasis was 67.6%(23/34), 75.0%(24/32),91.4%(32/35),93.8%(15/16) and 81.8%(9/11) respectively. Expression rate of tumor significantly increased compared with normal colonic mucosa (χ2=6.37, P＜0.05). The expression rate of the tumor in different groups, such as patients of different sex, serum CEA level, tumor size, location, histological grade and pathological stage, showed no difference (P＞0.05）.ConclusionThe expression rate of SSTR2 mRNA of colorectal adenocarcinoma increases. The expression rate does not correlate with the histological grade and pathological stage of the tumor.
【Abstract】ObjectiveTo investigate the inhibitory effects of somatostatin analogue (SSTA) on the colonic carcinoma cell growth in vitro and in vivo and its possible mechanism. MethodsThe somatostatin receptor type Ⅱ (SSTR2) mRNA of colonic carcinoma cell line HCT116 was detected by using RTPCR and hybridization in situ. The effects of octreotide (Oct) or NC-8-12 (specific agonist of SSTR2 ) on the proliferation of HCT116 was measured with MTT after HCT116 stimulated by insulin or epidermal growth factor (EGF) and incubated with Oct or NC-8-12 simultaneously for 24 hours. The expression of cyclin D1 was detected with flow cytometry. The HCT116 were implanted in nude mice subcutaneously and treated with Oct or NC-8-12. The tumor volume and tumor weight were measured according to schedule. Results①SSTR2 mRNA was detected in HCT116 and the tumor implanted in nude mice; ②Insulin and EGF increased the proliferation of HCT116 significantly, and this proliferation could be inhibited by Oct and NC-8-12 partially; ③Insulin increased the Cyclin D1 expression of HCT116, its level decreased slightly when treated with Oct or NC-8-12 but not significantly (Pgt;0.05); ④The weight and volume of implanted tumor in nude mice treated with Oct or NC-8-12 showed no significant difference compared with the control group (Pgt;0.05). ConclusionBoth Oct and NC-8-12 could inhibit the proliferation of colonic carcinoma cell line HCT116 in vitro, which indicated that SSTR2 may mediated the inhibition. Oct and NC-8-12 have no effect on the growth of implanted HCT116 in nude mice in this experiment.