Cervical Cancer (CC) is the fourth leading cause of cancer deaths in women worldwide and is associated directly with Human papillomavirus (HPV) infection. Many authors have reported that HPV can immortalize human cells without leading to cell transformation by itself. Thus, cervical carcinogenesis is a multistep process involving HPV infection and additional alterations. In 2005, canonical Wnt signaling pathway activation was proposed as a second hit during epithelial malignant transformation but this hypothesis remains controversial. However, it is undeniable that Wnt signaling pathway is altered during CC progression.
The Wnt signaling pathway participates in cell differentiation, proliferation, migration, cell polarity, and cell fate determination, playing an important role during embryogenesis, tissue regeneration, stem cell maintenance, homeostasis, and under pathologic conditions including cancer. At least three different pathways have been described: the canonical Wnt/β-catenin cascade, and two non-canonical pathways: the Planar cell polarity (PCP) pathway and the Wnt/Ca2+ pathway. Neither the 19 Wnt ligands nor the 10 Frizzled receptors described to date can be classified as activators of one or another signaling pathway. Indeed, although it appears that some ligands preferentially activate a specific pathway, factors such as cell context, receptors, and inhibitors require consideration.