胃癌组织SSTR亚型与P-ERK表达关系的研究

Study on the expression correlation between SSTR and P-ERK in the tissue of gastric cancer

目的研究磷酸化的细胞外信号调节激酶(P-ERK)与生长抑素受体(SSTR)在胃癌中表达的关系,探索SSTR在生长抑素(SS)抑癌机制中的作用途径。方法应用免疫组化法和Western blot法检测胃癌、癌旁及浅表性胃炎组织SSTR1、SSTR3和P-ERK的表达。结果SSTR1、SSTR3、P-ERK主要着色于胞质内,在癌旁及浅表性胃炎组织阳性细胞主要位于胃腺颈部及周围。胃癌组的SSTR1、SSTR3表达较浅表性胃炎及癌旁组明显减少(P<0.01)。胃癌组P-ERK的表达较浅表性胃炎及癌旁组增多(P<0.01)。Western blot显示,胃癌组SSTR1、SSTR3表达与P-ERK表达呈负相关关系(r=-0.504和-0.527,P均<0.05)。结论SS通过SSTR抑制胃癌的机制部分可能是经过MAPK-ERK信号通路进行的。

Objective To investigate the correlation of somatostatin receptor （SSTR） and phosphorilated extracellular signal - regulated kinase （ P - ERK） in the process of gastric cancer, and to probe into the action route of SSTR in the inhibition mechanisms of somatostatin （ SS ） on the of the growth of human gastric cancer. Methods Expression of SSTR1, SSTR3 and P - ERK in gastric cancerous tissues, their corresponding adjacent tissues and superficial gastritis tissues were determined by immmunobistochemistry （IHC） and Western blot. Results SSTR1, SSTR3, P - ERK were mainly stained in the cytoplasm of cancerous cells and normal gastric mucosal cells. The positive cells in cancer adjacent tissues and superficial gastritis tissues were mainly located in the gland isthmuses and their peripheral tissues. A lower level of expression of SSTR1, SSTR3 was detected in gastric cancer group than in superficial gastritis group and cancer adjacent tissues. There were statistic differences between these groups （ P 〈 0.01 ）. A higher level of expression of P - ERK was detected in the gastric cancer group than in superficial gastritis group and cancer adjacent tissues. There were statistic differences between these groups （ P 〈 0.01 ）. The expression of P - ERK in gastric cancer group was higher than that in two control groups. There were statistic differences between these groups. The statistic analysis of D value of SSTR1, SSTR3 and P - ERK by Western blot revealed a negative correlativity in the expression of SSTR1, SSTR3 and P - ERK （ r = - 0.504 and - 0.527 respectively, P 〈 0.05 ）. Conclusion The inhibition mechanisms of SS via SSTR on the growth of human gastric cancer may be in part through the signal pathway of MAPK - ERK.