Guan Weiqun, Yu Shifeng, Gao Yan
Department of Stomatology, Union Hospital, Fujian Medical University, Fuzhou 350001, China.
Zhonghua Kou Qiang Yi Xue Za Zhi. 2002 Jan;37(1):65-8.
To study the expression and significance of apoptosis-related protein p53, Bcl-2, and Bax during the development of oral squamous cell carcinoma (SCC).
The expression was observed in 10 normal oral epithelia, 48 dysplasia epithelia and 42 SCC by immunohistochemical evaluation.
In normal mucosa, the positive rate of p53, Bcl-2 and Bax were 0%, 20% and 60%. In dysplasia epithelia, the positive rate of p53 is increased (P < 0.05), the positive rate of Bcl-2 and Bax remained no significant change (P > 0.05), but the positive intensity in severe dysplasia was higher than in mild group. In SCC, the positive rate of Bcl-2 increased significantly (compared with dysplasia, P < 0.05), while the expression of Bax was decreased with the increase of SCC histological grade. Further analysis showed the correlation was evident in p53 and Bax in dysplasia, and in p53 and Bcl-2 in SCC.
In dysplasia, p53 gene mutation results in accumulation of dysplasia cells. In SCC, the cooperation of p53, Bcl-2 and Bax results in the progression of SCC. Apoptosis genes could work either independently or cooperatively.
研究凋亡相关蛋白p53、Bcl-2和Bax在口腔鳞状细胞癌（SCC）发生发展过程中的表达及意义。
采用免疫组织化学方法观察10例正常口腔上皮、48例发育异常上皮和42例SCC中上述蛋白的表达情况。
在正常黏膜中，p53、Bcl-2和Bax的阳性率分别为0%、20%和60%。在发育异常上皮中，p53阳性率升高（P < 0.05），Bcl-2和Bax阳性率无明显变化（P > 0.05），但重度发育异常组的阳性强度高于轻度组。在SCC中，Bcl-2阳性率显著升高（与发育异常相比，P < 0.05），而Bax的表达随SCC组织学分级升高而降低。进一步分析显示，在发育异常中p53与Bax相关，在SCC中p53与Bcl-2相关。
在发育异常中，p53基因突变导致发育异常细胞积聚。在SCC中，p53、Bcl-2和Bax共同作用导致SCC进展。凋亡基因可单独或协同发挥作用。
