RAS-mediated oncogenic signaling pathways in human malignancies
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Date
2018-03-01
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Abstract
Abnormally activated RAS proteins are the main oncogenic driver that governs the functioning of major signaling
pathways involved in the initiation and development of human malignancies. Mutations in RAS genes and
or its regulators, most frequent in human cancers, are the main force for incessant RAS activation and associated
pathological conditions including cancer. In general, RAS is the main upstream regulator of the highly conserved
signaling mechanisms associated with a plethora of important cellular activities vital for normal homeostasis.
Mutated or the oncogenic RAS aberrantly activates a web of interconnected signaling pathways including RAFMEK
(mitogen-activated protein kinase kinase)-ERK (extracellular signal-regulated kinase), phosphoinositide-3
kinase (PI3K)/AKT (protein kinase B), protein kinase C (PKC) and ral guanine nucleotide dissociation stimulator
(RALGDS), etc., leading to uncontrolled transcriptional expression and reprogramming in the functioning of a
range of nuclear and cytosolic effectors critically associated with the hallmarks of carcinogenesis. This review
highlights the recent literature on how oncogenic RAS negatively use its signaling web in deregulating the
expression and functioning of various effector molecules in the pathogenesis of human malignancies.