Knockdown of frizzled-7 inhibits cell growth and metastasis and promotes chemosensitivity of esophageal squamous cell carcinoma cells by inhibiting Wnt signaling.

A growing body of evidence suggests that frizzled-7 (FZD7) is an important oncogene in multiple human malignancies and is involved in regulating sensitivity to chemotherapeutic drugs. However, little is known about the expression and function of FZD7 in esophageal squamous cell carcinoma (ESCC). In this study, we aimed to investigate the functional significance of FZD7 in ESCC. Here, we found that both mRNA and protein expression levels of FZD7 were highly upregulated in ESCC cell lines. The knockdown of FZD7 inhibited cell growth, induced cell apoptosis, and suppressed cell migration and invasion of ESCC cells in vitro. Furthermore, knockdown of FZD7 promoted chemosensitivity to cisplatin in ESCC cells and suppressed the expression of multidrug resistance protein 1. Moreover, the silencing of FZD7 also significantly impeded the activation of Wnt signaling in ESCC cells. Taken together, our study reveals an oncogenic role of FZD7 in the progression of ESCC and suggests that FZD7 might serve as a potential therapeutic target for treatment of ESCC.