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目的：探讨口腔鳞癌发生的分子生物学机理。方法：采用Ｔａｋａｉ法研究２０例口腔鳞癌及其临近正常组织的蛋白激酶Ｃ（ＰｒｏｔｅｉｎｋｉｎａｓｅＣ，ＰＫＣ）及其抑制物（ＰｒｏｔｅｉｎｋｉｎａｓｅＣｉｎｈｉｂｉｔｏｒ，ＰＫＣＩ）活性。结果：与临近正常组织相比口腔鳞癌胞浆ＰＫＣ活性明显升高（Ｐ＜０．０１），而胞膜无明显变化（Ｐ＞０．０５）；与临近正常组织相比口腔鳞癌胞浆ＰＫＣＩ活性明显降低（Ｐ＜０．０１），而胞膜无明显变化（Ｐ＞０．０５）。结论：口腔鳞癌的发生与ＰＫＣ及ＰＫＣＩ在亚细胞水平活性变化密切相关。
Objective: To investigate the molecular biological mechanism of oral squamous cell carcinoma. Methods: Takai's method was used to study the protein kinase C (PKC) and its inhibitor (PKCI) activity in 20 cases of oral squamous cell carcinoma and its adjacent normal tissues. Results: The cytoplasmic PKC activity in oral squamous cell carcinoma was significantly higher than that in adjacent normal tissues (P <0.01), but there was no significant change in the cell membrane (P> 0.05). Compared with adjacent normal tissues, oral squamous cell carcinoma PKCI activity was significantly decreased (P <0.01), but no significant changes in the membrane (P> 0.05). Conclusion: The occurrence of oral squamous cell carcinoma is closely related to the changes of PKC and PKCI in subcellular level.