FAT Cadherine and Wnt Signaling in the Progression of Breast Cancer with Hyperglycemia

Abstract

Breast cancer has continued to be one of the most common causes of cancer death among females without sparing either those in modern societies or rural communities. Breast cancer is, in general, the uncontrolled cell growth in the mammary glands. This encompasses stromal and epithelial cells as the major cause of breast cancer. The disruption of communication between stromal and epithelial cells is one of the inducers of breast cancer. The mechanism surrounding this uncontrolled cell growth is postulated to be due to the role played by cadherin molecules and WNT signaling in mammary gland tumorogenesis and the hyperglycemia-driven modulation of the progression of breast cancer. Among different FAT cadherin molecules, repression of FAT4 mediates the Wnt signaling cascades, which regulate tissue homeostasis, vascularization, tumorigeneses, cell invasion, and metastasis. The epithelial-to-mesenchymal transition (EMT), which is promoted by transforming growth factor beta (TGF-beta) through the Wnt Signaling pathway, leads to the progression of breast cancer. This fundamental discussion may contribute to designing new signaling-targeted therapeutic approaches to mitigate breast cancer and associated factors for hyperglycemia.