肺癌组织中Cox-2和突变型P53蛋白与凋亡的相关性

CORRELATION OF COX-2 AND MUTATED P53 PROTEIN WITHAPOPTOSIS IN LUNG CANCER

目的研究Cox-2蛋白和凋亡相关蛋白突变型p53在肺癌组织中对凋亡的抑制作用,及其对预后的影响。方法应用DNA缺口末端标记技术和免疫组化方法检测116例肺癌患者组织中细胞凋亡、突变型p53和cox-2蛋白表达水平;并用cd34标记血管来计数肿瘤组织的微血管密度。结果116例肺癌中,细胞凋亡高表达56例(48.28%),突变型p53蛋白阳性47例(40.52%),cox-2蛋白阳性78例(67.24%)。Cox-2蛋白的表达与肿瘤TNM分期(P=0.014)及其中的淋巴结转移情况(P=0.009)密切相关,且阳性表达的肺癌组织中微血管密度明显高于阴性表达者(P=0.000),有统计学意义。COX模型多因素分析显示,淋巴结的转移(P=0.004)和cox-2蛋白的阳性表达(P=0.000)是本组肺癌患者的预后不良因素。结论Cox-2能增加突变型p53蛋白的表达,抑制凋亡,可作为判断肺癌患者预后不良的潜在指标。

Objective To investigate the prognostic significance of the expressions of Cox-2 and apoptosis related protein mutated p53, and their roles in suppressing apoptosis in lung cancer. Methods The positive expressions of apoptosis, Cox-2, mutated p53 and cd34 proteins were observed in 116 cases of lung cancer by using DNA nick end labeling （TUNEL） technique and immunohistochemical staining, and microvascular density was measured. Results In the specimens of 116 lung cancer, the high expression of cell apoptosis was seen in 56 cases （48.28%）, the positive rate of mutated p53 and cox-2 protein expressions were 47 （40. 52% ） and 78 （67. 24% ） respectively. The expression of cox-2 was related to tumor TNM staging （P =0. 014） and lymph node metastasis （P = 0. 009）, while microvascular density was significant higher in positive expression than in negative expression （P =0. 000） . COX model showed that lymph node metastasis （P =0. 004） and the positive rate of cox-2 protein （ P = 0. 000） were poor factors to the prognosis of lung cancer patients. Conclusion Protein cox-2 can improve the expression of mutated p53 and suppress apoptosis and can serve as a potential marker of prognosis in cancer.