In oral squamous cell carcinoma(OSCC), the mutation frequencies of subtype Harvey rat sarcoma virus(RAS), Kirsten RAS, and neuroblastoma RAS of the RAS gene are 11.2%(140/1 251), 4.5%(35/786), and 0.3%(1/375), respectively. RAS mutations occur mostly in 12, 13, and 61 codon sites and consistently generate active RAS, which can activate and rapidly accelerate the fibrosarcoma-mitogen-activated protein kinase and phosphatidylinositol-3-kinase-protein kinase B downstream signaling pathways. In these pathways, cells undergo aberrant proliferation and differentiation that can lead to malignancy. Hence, RAS and downstream signaling molecules are molecular therapeutic targets in OSCC. This review focuses on the mutation, activation mechanism, and therapeutic target of RAS in OSCC.
