Wnt signaling and plasticity of lung cancer cells

Abstract

Cancer cell plasticity includes their interconversion into various subtypes or entirely different cells through transdifferentiation. This allows the cells to survive in difficult microenvironments while remaining unresponsive to treatment. Plastic characteristics of cancer cells include increased metastasis, tumorigenesis, and chemoresistance. Though many pathways regulate these activities, this paper focuses on the Wnt signaling pathway. When Wnt is activated, the Axin is dephosphorylated, allowing the phosphorylation of ?-catenin (?-Cat) and the degradation of antigen-presenting cell (APC). This degradation is important because APC is classified as a tumor suppressor; therefore, when Wnt is on, tumorigenesis is more likely to occur. Lung cancer contains a subpopulation of cancer stem-like cells (CS-LCs), which are highly resistant to anticancer drugs and are a major catalyst for tumor recurrence. The Wnt signaling pathway, in conjunction with other pathways, is a key player in the development and maintenance of cancer stem cells, catalyzing increased chemoresistance and metastasis. The Wnt signaling pathway can sustain these CS-LCs with ?-Cat present in the pathway. In this review, we summarize the current knowledge surrounding the Wnt signaling pathway as well as its crosstalk with other pathways and their implications for cancer cell plasticity. Keywords: Chemoresistance, crosstalk, lung cancer, plasticity, tumorigenesis, Wnt signaling