Aberrant Signaling Pathways in Cancer Cells: Application of Nanomaterials

Abstract

Several signaling pathways trigger normal cellular activities. Few membrane proteins such as receptor tyrosine kinases (RTKs) bind extracellular messenger molecules such as hormones or growth factors (called ligands) and undergo a conformational change relaying the signal across the membrane to the receptor’s cytoplasmic domain. Subsequently, the membrane-bound protein is activated (by phosphorylation), for example, Ras in its active GTP-bound state. GTPase-activating proteins such as neurofibromin-1 (NF-1) deactivate (dephosphorylation) Ras by converting it to an inactive GDP-bound state. The activated protein interacts with several downstream effectors initiating cascades of enzymic activities through one of the pathways to regulate cellular activities, like cell division and growth, repair of damaged DNA, glycolysis, and apoptosis [2,3]. Dysregulation in these signal transduction pathways boons the cell’s capacity to proliferate independently of exogenous growthpromoting or growth-inhibitory signals, invade surrounding tissues and metastasize to distant sites, to resist apoptosis and other forms of cell death, metabolic activities in hypoxia, sustain with genetic instability, and to induce angiogenesis [4]. Proteins associated with these dysregulated pathways are currently under investigation as possible targets of various drugs to develop cancer therapy. In this article, we have reviewed three cell signaling pathways triggered by Ras and Wnt proteins and the NF-2 genes in connection with different Abstract