Gprotein-coupled estrogen receptor 30 and extracellular signal-regulated kinase 1/2 in endometrial adenocarcinoma

Abstract

Endometrial cancer which originates from the malignant proliferation and differentiation of endometrialepithelium cells, along with cervical cancer and ovarian cancer, are the three most malignant cancers inthereproductive system of females. The incidence of endometrial cancer ranked the second among themalignant cancers of reproductive system of females. Endometrial adenocarcinoma is the main pathologicalcategory, with an incidence of 20-30%. The current target treatment of endometrial adenocarcinoma isstill being explored. Therefore it is of great significance to study the expression of signal pathway and geneproteins in the cancerous development of endometrial epithelium cells and their invasion and metastasisprocess. To investigate the expression of gprotein-coupled estrogen receptor 30 (GPR30) and phosphorylatedextracellular signal-regulated kinase 1/2 (p-ERK1/2) in endometrial adenocarcinoma and its significance,the expressions of GPR30 and p-ERK1/2 in the tissues from 24 cases of endometrial adenocarcinoma, 24cases of endometrial atypical hyperplasia (EAH) and 24 cases of normal endometrium were detected usingstreptavidin-perosidase method. The results demonstrated that the positive expression rate of GPR30 in theEAH and endometrial adenocarcinoma group significantly increased, and the differences with the normalendometrium group had statistical significance (P<0.05). The positive expression rate of p-ERK1/2 was thehighest in the EAH group, and the difference with the normal endometrium group was statistically significant(P<0.05). The expression of GPR30 in endometrial cancer with different depth of myometrial invasion wassignificantly different; the deeper the myometrial invasion, the higher the positive expression rate (P<0.05).The expressions of GPR30 and p-ERK1/2 was in no correlation with the other clinicopathological parameters.There was no correlation between the expressions of GPR30 and p-ERK1/2 in the normal endometrium tissues(rs=0.032, P>0.05), but there was a positive correlation between the expressions of GPR30 and p-ERK1/2 inthe EAH and endometrial adenocarcinoma group (rs=0.601, 0.557, P<0.05). Thus, it can be concluded thatGPR30 may play its regulatory role in endometrial adenocarcinoma via p-ERK1/2 signal pathway.