Part of the book: Glycosylation
Cancer cells are remarkably resilient to therapies aimed at their elimination. The exploration of pathways that sustain cancer cells and that allow cancer cells to become resistant has revealed new avenues for chemotherapeutic development, as well as rational approaches to combination therapies based on existing treatment options. Several signaling pathways, such as Wnt, phosphoinositide 3-kinase (PI3K), and Ras-Raf-MEK, constitute integrated networks that work together to maintain cellular homeostasis under basal conditions and to drive cell-mass accumulation and cell cycle progression in the presence of appropriate mitogenic stimuli. During cancer development, these pathways are corrupted in malignant cells to maintain viability and proliferative activity under environmentally stressful conditions such as limited growth factors, oxygen, and nutrients that drive normal cells into quiescence or death. Importantly, dysfunction within any one of these pathways results in compensatory responses from the other networks. Thus, biological research is gradually shifting toward more general approaches that target entire pathways rather than isolated components and integrate those pathways into biological networks.
Part of the book: Colorectal Cancer
Aberrant Wnt signaling is a hallmark of many cancer types such as colon cancer. However, the effect of altered Wnt signaling is not only restricted to cancer cells but also dynamically interacts with a tumor microenvironment and has the ability to directly regulate the anti-tumor immune response. It has been reported that tumors induce immune tolerance through the activation of canonical Wnt signaling in dendritic cells promoting T regulatory responses, and also that both canonical and noncanonical Wnt proteins program dendritic cell responses for tolerance. Thus, the Wnt signaling pathway may be a novel and promising therapeutic target for anticancer immunotherapy. In this review, we will discuss the molecular mechanisms involved in immune cell response regulation mediated by canonical and noncanonical Wnt signaling.
Part of the book: Cell Signalling