Correlation between the expressions of gastrin, somatostatin and cyclin and cyclin-depend kinase in colorectal cancer.

aimTo explore the correlation between the expressions of gastrin (GAS), somatostatin (SS) and cyclin, cyclin-dependent kinase (CDK) in colorectal cancer, and to detect the specific regulatory sites where gastrointestinal hormone regulates cell proliferation.

methodsSeventy-nine resected large intestine carcinomatous specimens were randomly selected. Immunohistochemical staining for GAS, SS, cyclin D1, cyclin E, cyclin A, cyclin B1, CDK2 and CDK4 was performed according to the standard streptavidin-biotin-peroxidase (S-P) method. According to the semi-quantitative integral evaluation, SS and GAS were divided into high, middle and low groups. Cyclin D1, cyclin E, cyclin A, cyclin B1, CDK2, CDK4 expressions in the three GAS and SS groups were assessed.

resultsThe positive expression rate of cyclin D1 was significantly higher in high (78.6%, 11/14) and middle GAS groups (73.9%, 17/23) than in low GAS group (45.2%, 19/42) (P<0.05, c2(high vs low) = 4.691; P<0.05, c2(middle vs low) = 4.945). The positive expression rate of cyclin A was significantly higher in high (100%, 14/14) and middle GAS groups (82.6%, 19/23) than in low GAS group (54.8%, 23/42) (P<0.01, c2(high vs low) = 9.586; P<0.05, c2(middle vs low) = 5.040). The positive expression rate of CDK2 was significantly higher in high (92.9%, 13/14) and middle GAS groups (87.0%, 20/23) than in low GAS group (50.0%, 21/42) (P<0.01, c2(high vs low) = 8.086; P<0.01, c2(middle vs low) = 8.715). The positive expression rate of CDK4 was significantly higher in high (78.6%, 11/14) and middle GAS groups (78.3%, 18/23) than in low GAS group (42.9%, 18/42) (P<0.05, c2(high vs low) = 5.364; P<0.01, c2(middle vs low) = 7.539). The positive expression rate of cyclin E was prominently higher in low SS group (53.3%, 24/45) than in high (9.1%, 1/11) and middle (21.7%, 5/23) SS groups (P<0.05, c2(high vs low) = 5.325; P<0.05, c2(middle vs low) = 6.212). The positive expression rate of CDK2 was significantly higher in low SS group (77.8%, 35/45) than in high SS group (27.3%, 3/11) (P<0.01, c2(high vs low) = 8.151). There was a significant positive correlation between the integral ratio of GAS to SS and the semi-quantitative integral of cyclin D1, cyclin E, cyclin A, CDK2, CDK4 (P<0.05, (D1)r(s) = 0.252; P<0.01, (E)r(s) = 0.387; P<0.01, (A)r(s) = 0.466; P<0.01, (K2)r(s) = 0.519; P<0.01, (K4)r(s) = 0.434).

conclusionThe regulation and control of gastrin, SS in colorectal cancer cell growth may be directly related to the abnormal expressions of cyclins D1, A, E, and CDK2, CDK4. The regulatory site of GAS in the cell cycle of colorectal carcinoma may be at the G(1), S and G(2) phases. The regulatory site of SS may be at the entrance of S phase.