BACKGROUND:Recent studies have confirmed that the expression of Ezrin,hepatocyte growth factor(HGF)and its receptor(C-met)is related to the genesis,progress,invasion and metastasis of some malignant tumors.Researches have also found that the biological function of Ezrin is closely related to HGF/C-met in malignant tumors.However,there is no report on the expression levels of Ezrin,HGF and C-met in rat pancreatic cancer induced by dimethylbenzanthracene (DMBA).This study aimed to detect the expression of Ezrin, HGF and C-met in rat pancreatic cancer and non-cancerous pancreatic tissues,and assess its effect in cancer induction by DMBA. METHODS:Ninety Sprague-Dawley rats were divided into 3 groups randomly:40 in a pancreatic cancer model group (group A),40 in a trichostatin A(TSA)intervention group (group B),and 10 in a control group(group C).DMBA was directly implanted into the parenchyma of rat pancreas in group A+group B.The rats of group B were treated with 1 ml of TSA saline solution(1μg/ml)via intraperitoneal injection weekly.The carcinogenesis of rats executed within 3-5 months in groups A and B was observed by macrograph and microscopy. Meanwhile,the rats in group C were executed within 5 months. The EnVision TM immunohistochemistry for detecting the expression levels of Ezrin,HGF and C-met was used in paraffinembedded sections of the pancreatic specimens. RESULTS:The incidence of pancreatic cancer in group A was 48.6%and in group B 33.3%.The maximal diameter of tumor mass was significantly larger in group A than that in group B(P<0.05).No pathological changes were observed , in the pancreas of group C and other main organs of groups A and B.The positive rates of Ezrin,HGF and C-met were significantly higher in ductal adenocarcinoma than in non- cancerous pancreatic tissues of groups A and B(P<0.01).The positive rates of Ezrin,HGF and C-met were significantly higher in ductal adenocarcinoma of group A than those in non- cancerous pancreatic tissues of group A(P<0.05),but there was no significant difference in group B(P>0.05).The positive rates of Ezrin,HGF and C-met in non-cancerous pancreatic tissues proved mild to severe atypical hyperplasia of the ductal epithelia.The pancreas of group C and 2 cases of fibrosarcoma showed the negative expression of Ezrin,HGF and C-met.There was a trend of consistency in the expression of Ezrin,HGF and C-met in ductal adenocarcinoma(P<0.05 or P<0.01). CONCLUSIONS:DMBA directly implanted into the parenchyma of the pancreas can produce a model of pancreatic cancer with a high incidence in a short time.TSA might inhibit the carcinogenesis and growth of pancreatic cancer,and its effects may be related to the inhibition of the expression of Ezrin,HGF and C-met during the process.Ezrin,HGF and C-met may have positive effects on the carcinogenesis of rat pancreas. BACKGROUND: Recent studies have confirmed that the expression of Ezrin, hepatocyte growth factor (HGF) and its receptor (C-met) is related to the genesis, progress, invasion and metastasis of some malignant tumors. Researches have also found that the biological function Of Ezrin is closely related to HGF / C-met in malignant tumors. However, there is no report on the expression levels of Ezrin, HGF and C-met in rat pancreatic cancer induced by dimethylbenzanthracene (DMBA). This study aimed to detect the expression of Ezrin, HGF and C-met in rat pancreatic cancer and non-cancerous pancreatic tissues, and assess its effect in cancer induction by DMBA. METHODS: Ninety Sprague-Dawley rats were divided into 3 groups randomly: 40 in a pancreatic cancer model group A, 40 in a trichostatin A (TSA) intervention group (group B), and 10 in a control group (group C). DMBA was directly implanted into the parenchyma of rat pancreas in group A + group B. The rats of group B were treated with 1 ml of TSA saline solutio Within 1 to 5 months in groups A and B was observed by macrograph and microscopy. Meanwhile, the rats in group C were executed within 5 months. The EnVision ™ immunohistochemistry for detecting the expression levels of Ezrin, HGF and C-met was used in paraffin embedded sections of the pancreatic specimens. RESULTS: The incidence of pancreatic cancer in group A was 48.6% and in group B 33.3%. The maximal diameter of tumor mass was significantly larger in group A than that in group B (P <0.05) .No pathological changes were observed, in the pancreas of group C and the other main organs of groups A and B. The positive rates of Ezrin, HGF and C-met were significantly higher in ductal adenocarcinoma than in non-cancerous pancreatic tissues of groups A and B (P <0.01). The positive rates of Ezrin, HGF and C-met were significantly higher in ductal adenocarcinoma of group A than those in non- cancerous pancreatic tissues of group A (P <0.05), but there was no significant difference in group B (P> 0.05). The positive rates of Ezrin, HGF and C-met in non-cancerous pancreatic tissues proved mild to severe atypical hyperplasia of the ductal epithelia. of group C and 2 cases of fibrosarcoma showed the negative expression of Ezrin, HGF and C-met. There was a trend of consistency in the expression of Ezrin, HGF and C-met in ductal adenocarcinoma (P <0.05 or P <0.01) CONCLUSIONS: DMBA directly implanted into the parenchyma of the pancreas can produce a model of pancreatic cancer with a high incidence in a short time. TSA might inhibit the carcinogenesis and growth of pancreatic cancer, and its effects may be related to the inhibition of the expression of Ezrin, HGF and C-met during the process. Ezrin, HGF and C-met may have positive effects on the carcinogenesis of rat pancreas.