Vairaktaris Eleftherios, Goutzanis Lambros, Kalokerinos Giorgos, Yannopoulos Athanasios, Yapijakis Christos, Vassiliou Stavros, Spyridonidou Sofia, Vylliotis Antonis, Nkenke Emeka, Lazaris Andreas C, Tesseromatis Christina, Patsouris Efstratios
Department of Oral and Maxillofacial Surgery, University ofAthens Medical School, Athens, Greece.
In Vivo. 2007 Jul-Aug;21(4):615-21.
The expression of N-ras and ets-1 proteins was investigated in an experimental model of chemically-induced carcinogenesis in normal and diabetic (type I) Sprague-Dawley rats.
Tissue sections ranging from normal mucosa to moderately-differentiated oral squamous cell carcinoma were studied using monoclonal antibodies against N-ras and ets-1 proteins.
In diabetic rats, N-ras expression increased with tumor advancement, while in normal rats N-ras was not detected in initial stages of oral oncogenesis and increased only in well-differentiated OSCC. The same pattern of elevated ets-1 expression was observed both in diabetic and normal rats, but in cancerous stages this expression was higher in diabetic than in normal rats.
It seems that diabetes may contribute to increased cell proliferation due to N-ras constitutive activation, as well as to enhanced invasion and metastatic potential by increasing ets-1 levels.
在正常和糖尿病（I型）斯普拉格-道利大鼠化学诱导致癌的实验模型中，研究了N-ras和ets-1蛋白的表达。
使用抗N-ras和ets-1蛋白的单克隆抗体，研究了从正常黏膜到中度分化口腔鳞状细胞癌的组织切片。
在糖尿病大鼠中，N-ras表达随肿瘤进展而增加，而在正常大鼠中，口腔肿瘤发生的初始阶段未检测到N-ras，仅在高分化口腔鳞状细胞癌中增加。在糖尿病大鼠和正常大鼠中均观察到ets-1表达升高的相同模式，但在癌阶段，糖尿病大鼠中的这种表达高于正常大鼠。
糖尿病似乎可能由于N-ras的组成性激活而导致细胞增殖增加，以及通过增加ets-1水平而增强侵袭和转移潜能。
