Expression of miR-181a and CA125 and their correlation in human type I and II endometrial carcinoma / 解放军医学杂志

ABSTRACT

Objective To investigate the expression and correlation of microRNA-181a (miR-181a) and CA12S in human types I and II endometrial carcinomas. Methods A total of 78 formalin-fixed and paraffin-embedded endometrium tissue specimens were used in the present study, and they were supplied by Xiaolan People's Hospital affiliated to Southern Medical University, Southern Hospital and Zhongshan Hospital affiliated to Zhongshan University during Jan. 2011 to Dec. 2013. Among them, 13 were determined as normal endothelium by pathological and examination with immunohistochemical staining, 18 were endometrial hyperplasia, and 47 of them diagnosed were as endometrial carcinoma (type I 37 and type E 10). Total RNA was extracted from each of the specimens, and then the expression of miR-181a was determined by real-time PCR, and the expression of CA125 was detected by immunohistochemical staining. Results The expression levels of both miR-181a and CA125 were obviously higher in type I and II endometrial carcinoma tissues than in normal tissue (P<0.05). In addition, the expression of miR-181a was significantly higher in type II endometrial carcinoma than in type I endometrial carcinoma and endometrial hyperplasia tissues (P<0.05). Moreover, it was found that the expression of miR-181a increased gradually from that of normal endometrium to endometrial hyperplasia and then endometrial carcinoma, with statistically significant difference among them (P<0.05). In addition, there was also a significant difference in the expression of CA12S in different types of endometrial carcinoma (P<0.05). Correlation analysis showed that the expressions of miR-181a and CA12S were negatively correlated with each other in the process of carcinogenesis of endometrium (P<0.05). Conclusion There is a difference in expression of miR-181a between type I and type II endometrial carcinoma, and it may be related to the development and progression of endometrial carcinoma. The mechanism may be related to the expression of CA12S as regulated by miR-181a in the process of endometrial carcinogenesis, but the specific mechanism still needs further validation with experiments on the cellular level.