wnt5a is strongly expressed at the leading edge in non-melanoma skin cancer, forming active gradients, while canonical wnt signalling is repressedwnt5a强烈表达non-melanoma皮肤癌的前缘,形成活跃的梯度,而规范wnt信号是压抑的.pdfVIP

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2017-09-12 发布于上海
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wnt5a is strongly expressed at the leading edge in non-melanoma skin cancer, forming active gradients, while canonical wnt signalling is repressedwnt5a强烈表达non-melanoma皮肤癌的前缘,形成活跃的梯度,而规范wnt信号是压抑的.pdf

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wnt5a is strongly expressed at the leading edge in non-melanoma skin cancer, forming active gradients, while canonical wnt signalling is repressedwnt5a强烈表达non-melanoma皮肤癌的前缘,形成活跃的梯度,而规范wnt信号是压抑的

Wnt5a Is Strongly Expressed at the Leading Edge in Non- Melanoma Skin Cancer, Forming Active Gradients, while Canonical Wnt Signalling Is Repressed Celine Pourreyron1,3, Louise Reilly1,3, Charlotte Proby1,2,3, Andrey Panteleyev 1,3, Colin Fleming2,4, Kathleen McLean3,5, Andrew P. South1,3, John Foerster2,4* 1 Medical Research Institute, College of Medicine, Dentistry, and Nursing, University of Dundee, Dundee, Scotland, 2 Department of Dermatology, College of Medicine, Dentistry, and Nursing, University of Dundee, Dundee, Scotland, 3 Cancer Research UK Cancer Centre Dundee, College of Medicine, Dentistry, and Nursing, University of Dundee, Dundee, Scotland, 4 Education Division, College of Medicine, Dentistry, and Nursing, University of Dundee, Dundee, Scotland, 5 Tayside Tissue Bank, College of Medicine, Dentistry, and Nursing, University of Dundee, Dundee, Scotland Abstract Wnt5a is one of the so-called non-canonical Wnt ligands which do not act through b-catenin. In normal development, Wnt5a is secreted and directs the migration of target cells along concentration gradients. The effect of Wnt5a on target cells is regulated by many factors, including the expression level of inhibitors and receptors. Dysregulated Wnt5a signalling facilitates invasion of multiple tumor types into adjacent tissue. However, the expression and distribution of Wnt5a in cutaneous squamous cell carcinoma (SCC) and basal cell carcinoma (BCC), as well as the effect of Wnt5a on keratinocyte migration has not been studied in detail to date. We here report that Wnt5a is upregulated in SCC and BCC and localised to the leading edge of tumors, as well as tumor-associated fibroblasts. The Wnt5a-triggered bundling of its receptor Fzd3 provides evidence of Wnt5a concentration gradients projecting into the tumor. In vitro migration assays show that Wnt5a concentration g