Rabbit Anti-Human FZD1 (N-terminal) Polyclonal antibody

The Wnt family is involved in tumorigenesis of several tissues. In ovarian cancer, the role played by Writs and its pathways is not clearly defined. In order to analyze the canonical and noncanonical Writ pathway in normal ovary, benign ovarian tumor and ovarian cancer, we evaluated the immunohistochemical expression of Wnt1, Frizzled-1 (FZD1), Wnt5a, Frizzled-5 (FZD5) and B-catenin. Ovarian specimens were obtained from surgeries performed between 1993 and 2004. The patients were divided in three groups: group A, epithelial ovarian cancer (n=38); group B, benign epithelial neoplasia (n=28); and group C, normal ovaries (n=26). Immunoreactivity for Wnt1, FZD1, Wnt5a, FZD5 and B-catenin was scored for each group. The proportion of Wnt1 positive women in group A (29.4%) was significantly higher than in group B (4.3%) and C (9.1%) (p=0.020). The proportion of FZD1 positive patients in group C (54.5%) was significantly lower than in group A (97.1%) and B (90.0%) (p<0.001). The proportion of Wnt5a positive women was significantly higher for group A (80.0%) compared to group B (25.0%) and C (27.3%) (p<0.001). The proportion of beta-catenin positive patients in group C (95.8%) was significantly higher than group B (52.4%) (p=0.004). Comparison of the survival curves in group A according to Wnt5a expression showed a significant difference between positive and negative patients, whereas the Wnt5a positive women showed worse results (p=0.050). Our findings suggest that the pathways related to Wnt5a have an important role in ovarian malignant neoplasia. Furthermore, Wnt5a was found to be a predictor of poor prognosis for ovarian cancer.

Kashin-Beck disease (KBD), an endemic osteochondropathy, is characterized by cartilage degeneration which is caused by abnormal catabolism in the extracellular matrix (ECM). In this study, we investigated the expression of the Wnt/beta-catenin signaling pathway in KBD pathogenesis. Among the proteins involved in the Wnt/beta-catenin signaling pathway, WNT-3A, FZD1, SOX9, and beta-catenin were up-regulated, while FRZB was down-regulated in KBD cartilage. C28/I2 cells were evaluated for cell viability using the MTT assay after exposure to T-2 toxin, a suspicious environmental pathogenic factors of KBD. C28/I2 cells were treated with different intervening concentrations (0.001 mu g/mL,0.005 mu g/mL and 0.01 mu g/mL) of T-2 toxin for 24 h. The expression of FZD1 and CTNNB1 (i.e.,(beta-catenin) was significantly reduced and SOX9 expression was significantly increased in chondrocytes after treatment with different intervening concentrations of T-2 toxin. Our results indicate that alterations in the Wnt/beta-catenin signaling pathway in articular cartilage play an important role in the onset and pathogenesis of KBD.