Application Abstract: Endometrial adenocarcinoma continues to be the most common malignancy of the female genital tract over the past years.Immunohistochemistry,western blotting and ElISA were used to detect the MAPK signal pathway change in the progression of endometrial adenocarcinoma.The regulation of estrogen receptor,GPR30 and MAPK pathway,and its relation to clinicopathologic factor and malignant biological behaviour of endometrial adenocarcinoma was also investigated.The study showed that:①there was no difference for the expression of t-ERK1/2 and p-ERK1/2 among normal endometrium,hyperplasis endometrium and EC.The expression of t-ERK1/2 and p-ERK1/2 has no relation to FIGO stage,grade and myometrial invasion,lymph node metastasis(p>0.05).②GPR30 was highly expressed in endometrial adenocarcinoma,and its expression was correlated to the grade of the cancer.③The MAPK pathway was activated after treated with estrogen and inhibited after treated with tamoxifen independent with estrogen receptor.④GPR30 was expressed both in ERα positive endometrial cancer cell line RL95-2 and ERα negative endometrial cancer cell line KLE.Both estrogen and GPR30 activator could activate MEK/ERK MAPK pathway in cell line RL95-2 and KLE.⑤Estrogen could promote the KLE and RL95-2 proliferation and stimulate matrix metalloproteinase production and activity via the GPR30-mediated MEK/ERK mitogen-activated protein kinase pathway.
