Abstract
WNT family member 6 (WNT6) is a member of the highly conserved WNT protein family. It plays an essential role in the normal development process, not only in embryonic morphogenesis, but also in post-natal homeostasis. WNT6 functions in mice and humans. This review summarizes the current findings on the biological functions of WNT6, describing its involvement in regulating embryogenesis, decidualization, and organ development. Aberrant WNT6 signaling is related to various pathologies, such as promoting cancer development, lung tuberculosis, and kidney fibrosis and improving the symptoms of Rett syndrome (RTT). Thus, due to its various functions, WNT6 has great potential for in-depth research. This work not only describes the signaling mechanism and function of WNT6 under physiological and pathological conditions, but also provides a theoretical basis for targeted therapy.
Highlights
WNT family member 6 (WNT6), a member of the Wingless/integrase 1 (WNT) family comprising at least 19 members in mammals, is a secreted glycoprotein
WNT6 protein activates and upregulates phosphorylated Jun N-terminal kinase (JNK) and c-Jun mRNA in Human dental papilla cells (hDPCs) to induce migration and differentiation (Li et al, 2014). These results indicate that WNT6 is not involved in the proliferation of hDPCs, it is involved in the specific differentiation and migration of hDPCs through the β-catenin-independent WNT pathway
WNT6 overexpression increases the activity of the promoters of both insulin-like growth factor-1 (IGF-1) and brainderived neurotrophic factor (BDNF) in a dose-dependent manner in HEK293T cells, and can restore the level of bdnf and igf-1 mRNA in mouse, and suppress the binding of cAMP-responsive element binding protein (CREB) to IGF-1 and BDNF to increase the expression of two genes
Summary
WNT family member 6 (WNT6), a member of the Wingless/integrase 1 (WNT) family comprising at least 19 members in mammals, is a secreted glycoprotein. Ribosomal protein S6 kinase 1 (S6K1), another molecule that stimulates adipogenesis, is activated and translocates into the nucleus to suppress the transcription of WNT6, WNT10a, and WNT10b genes by phosphorylating histone H2B (Yi et al, 2016). Wnt6 mRNA induces expression of the c-Myc gene in macrophages, through a β-catenin independent pathway, to promote macrophage proliferation (Varlakhanova and Knoepfler, 2009; Schaale et al, 2013).
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