Inter J Stomatol ›› 2015, Vol. 42 ›› Issue (2): 237-242.doi: 10.7518/gjkq.2015.02.027

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Rat sarcoma virus gene in oral squamous cell carcinoma

Liu Min1,2, Wang Xuxia1,3   

  1. 1. Dept. of Oral and Maxillofacial Surgery, Hospital of Stomatology, Shandong University, Jinan 250012, China; 2. Dept. of Stomatology, The Affiliated Hospital of Taishan Medical College, Taian 271016, China; 3. Shandong Provincial Key Laboratory of Oral Biomedicine, Jinan 250012, China
  • Received:2014-02-26 Revised:2014-08-19 Online:2015-03-01 Published:2015-03-01

Abstract:

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.

Key words: oral squamous cell carcinoma, rat sarcoma virus gene, gene mutation


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