Fzd7, short for Frizzled class receptor 7, is a crucial receptor in the Wnt signaling pathway. The Wnt pathway is fundamental in numerous biological processes such as cell proliferation, differentiation, and development. Aberrant activation of this pathway has been linked to various diseases, especially cancers [1,2,3,4,5,6,7,9,10]. Genetic models, like gene knockout (KO) or conditional knockout (CKO) mouse models, are valuable for studying Fzd7's function.

In cancer research, multiple studies have highlighted Fzd7's role. In intrahepatic cholangiocarcinoma, circACTN4 recruits YBX1 to initiate FZD7 transcription, promoting tumor progression [1]. In endometriosis, FZD7 is highly expressed compared to normal endometrium and may drive disease progression [2]. In melanoma, the WNT11-FZD7-DAAM1 signaling axis is crucial for tumor-initiating abilities and amoeboid invasion [3]. In pancreatic cancer, Fzd7/Wnt7b signaling contributes to stemness and chemoresistance, and FZD7 accelerates hepatic metastases by promoting EMT and strengthening cell stemness [4,6]. In ovarian cancer, FZD7 is overexpressed, and a specific antibody-drug conjugate can induce tumor regression. Also, FZD7 marks platinum-tolerant cancer cells susceptible to ferroptosis, and the FZD7-TWIST1 axis is responsible for anoikis resistance and tumorigenesis [5,9,10].

In non-cancer research, in immature porcine Sertoli cells, FZD7, regulated by non-CpG methylation, is important for cell proliferation [8].

In conclusion, Fzd7, through its involvement in the Wnt signaling pathway, plays diverse and significant roles in both normal biological processes such as cell proliferation in Sertoli cells and disease conditions, particularly various cancers. The use of KO/CKO mouse models, though not directly detailed in the provided references, would further enhance our understanding of its functions in these specific biological and disease-related contexts.