ABSTRACT
This study examined the expression of cell adhesion molecule 1 (CADM1) in pancreatic cancer and the possible mechanism. The expression of CADM1 was detected by immunohistochemistry in tissues of pancreatic cancer, pancreatitis, and normal pancreas. The plasmid pcDNA3.1-Hygro(+)/CADM1 was transfected into PANC-1 cells (a pancreatic cancer cell line). The expression of CADM1 in the transfected cells was determined by RT-PCR and Western blotting. Cell growth was measured by the MTT method and cell apoptosis by flow cytometry. The results showed that CADM1 was weakly expressed in tissues of pancreatic cancer in contrast to its high expression in normal pancreatic and pancreatitis tissues. The expression level of CADM in pancreatic caner was intensely correlated with the differentiation degree, lymph node metastasis and TNM stages. The growth of CADM1-transfected PANC-1 cells was significantly suppressed in vitro by a G1 cell cycle arrest and apoptosis occurrence. It was concluded that re-expression of CADM1 inhibits the growth of pancreatic cancer cells and induces their apoptosis in vitro. As a tumor suppressor gene, CADM1 plays an important role in the occurrence, progression and metastasis of pancreatic cancer.
ABSTRACT
Objective To investigate the expressions of PI3K, AKT and MRP protein in pancreatic carcinoma and to determine the clinicopathological significance and the correlation among three protein expressions. Methods The immunohistochemical method was used to detect the expressions of PI3K, AKT and MRP in forty three pancreatic carcinoma, nine chronic pancreatitis and eight normal pancreatic tissue samples. Results The positive expression rates of PI3K, AKT and MRP were 46.51%, 55.81% and 39.53%, respectively in pancreatic carcinoma, which were remarkably higher than those in normal pancreatic tissue and in chronic pancreatitis (P<0.01 and P<0.05, respectively). The aberrant expression of PI3K, AKT and MRP were associated with lymph node metastasis and TNM stages (P<0.05). The abnormal expression rate in both MRP and PI3K was 32.56%, the normal expression rate of both MRP and PI3K was 46.51%, and there was positive correlation between the expression of MRP and PI3K(r=0.581, P<0.01). The abnormal expression rate of both MRP and AKT was 32.56%, the normal expression rate was 37.21%, and there was a positive correlation between MRP and PI3K (r=0.432,P<0.05). The abnormal expression rate of both MRP and PI3K was 37.21%, the normal expression rate of both MRP and PI3K was 32.56%, there was also a positive correlation between MRP and PI3K (r=0.306,P<0.05). Conclusions The expressions of PI3K, AKT and MRP were up-regulated in pancreatic carcinoma. The expressions of PI3K and AKT may be related to the lymph node metastasis and TNM staging.