Background: Wnt7a is a secreted glycoprotein that regulates normal cellular proliferation and differentiation, as well as tumorigenesis and progression. The aim of the present study was to detect the level of expression of Wnt7a in endometrial cancer and explore its role in progression and prognosis of endometrial cancer.
Methods: Immunohistochemistry was used to examine the expression of Wnt7a in 244 endometrial cancer specimens, in 48 benign endometrial lesion specimens, and 43 normal endometrium specimens. χ2 Analysis, Kaplan-Meier analysis and log-rank test, and multivariate Cox proportional hazards analysis were applied for statistical analysis.
Results: Wnt7a was overexpressed in endometrial cancer compared with normal endometrium and benign endometrial lesion (both P < 0.001). Wnt7a expression was correlated with histological grade, International Federation of Gynecology and Obstetrics stage, depth of myometrial invasion, vascular/lymphatic invasion, and lymph node metastasis. The results of Kaplan-Meier analysis indicated that Wnt7a expression was associated with overall survival (OS) and disease-free survival (DFS) of endometrial cancer. The survival of negative expression Wnt7a group had longer OS and DFS compared with the group with positive expression. The difference was significant (both P < 0.001, log-rank test). Multivariate Cox regression analysis revealed that Wnt7a expression status was an independent prognostic factor for both OS and DFS (P = 0.034 and P = 0.009, respectively) of patients with endometrial cancer.
Conclusions: Overexpression of Wnt7a may contribute to the progression of endometrial cancer and thus may serve as a new biomarker to predict the prognosis of endometrial cancer.
Departments of *Gynecology and †Breast Surgery, The Affiliated Tumor Hospital, Harbin Medical University, Harbin, China.
Address correspondence and reprint requests to Ge Lou, MD, Department of Gynecology, The Affiliated Tumor Hospital, Harbin Medical University, Baojian Rd 6, Nangang District, Harbin 150081, China. E-mail: email@example.com.
This work was supported by Science Foundation of the Affiliated Tumor Hospital of Harbin Medical University (no. JJ-2010-17), Heilongjiang Province, China.
The authors declare no conflicts of interest.
Received August 24, 2012
Accepted November 4, 2012