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目的前列腺素E2(prostaglandin E2,PGE2)可以通过促进癌细胞的增殖、抑制癌细胞的凋亡、促进癌细胞的转移等方式促进口腔鳞癌的发生发展,但关于其具体作用机制罕见报道。因此,本研究旨在检测口腔鳞状细胞癌组织和相应癌旁组织中花生四烯酸(arachidonic acid,AA)及前列腺素E2受体3亚型(E-prostanoid 3,EP3)的表达。方法选取南方医科大学南方医院2013-05-01-2015-05-01行手术治疗的口腔鳞癌患者40例,将口腔鳞状细胞癌组织作为观察组(40例),相应癌旁组织作为对照组(40例)。ELISA方法检测AA的表达,Real-time PCR方法检测EP3受体mRNA的表达,免疫组织化学染色方法检测EP3受体蛋白的表达。结果与癌旁组织相比,AA在口腔鳞状细胞癌组织中的表达明显升高。40例口腔鳞癌组织中AA的平均质量分数为(477.4±39.84)pg/g,40例癌旁组织中AA的平均质量分数为(38.4±4.92)pg/g,差异有统计学意义,t=3.146,P=0.001。与癌旁组织相比,鳞癌组织中EP3受体mRNA的表达明显降低。40例鳞癌组织EP3受体mRNA的相对平均表达量为0.43±0.15,差异有统计学意义,t=2.365,P=0.011。与癌旁组织相比,鳞癌组织中EP3受体蛋白的表达明显降低,20例癌旁组织呈阳性表达,而18例鳞癌组织呈弱阳性表达,差异有统计学意义,T=-114,P=0.016。结论口腔鳞状细胞癌组织中,AA表达量的显著上调,EP3受体表达量的显著下调,可能在口腔鳞状细胞癌的发生发展过程中发挥了重要作用。
Objective Prostaglandin E2 (PGE2) can promote the development of oral squamous cell carcinoma by promoting the proliferation of cancer cells, inhibiting the apoptosis of cancer cells and promoting the metastasis of cancer cells. However, its specific mechanism of action is rarely reported. Therefore, the aim of this study was to detect the expression of arachidonic acid (AA) and prostaglandin E2 receptor subtype 3 (EP3) in oral squamous cell carcinoma tissues and corresponding paracancerous tissues. Methods Southern Hospital of Southern Medical University 2013-05-01-2015-05-01 Surgical treatment of oral squamous cell carcinoma in 40 patients, the oral squamous cell carcinoma as the observation group (40 cases), the corresponding paracancerous tissue as a control Group (40 cases). The expression of EP3 receptor mRNA was detected by ELISA and the expression of EP3 receptor protein by immunohistochemical staining. Results The expression of AA in oral squamous cell carcinoma was significantly higher than that in paracancerous tissues. The average mass fraction of AA was (477.4 ± 39.84) pg / g in 40 cases of oral squamous cell carcinoma, and the average mass fraction of AA in 40 paracancerous tissues was (38.4 ± 4.92) pg / g, the difference was statistically significant = 3.146, P = 0.001. The expression of EP3 receptor mRNA in squamous cell carcinoma was significantly lower than that in paracancerous tissues. The relative average expression level of EP3 receptor mRNA in 40 squamous cell carcinomas was 0.43 ± 0.15, with a significant difference (t = 2.365, P = 0.011). The expression of EP3 receptor protein in squamous cell carcinoma was significantly lower than that in paracancerous tissues, while the expression of EP3 receptor protein was significantly lower in 20 cases of paracancerous tissues than in paracancerous tissues, while it was weakly positive in 18 cases of squamous cell carcinoma (T = -114 , P = 0.016. Conclusion The overexpression of AA and the down-regulation of EP3 receptor expression in oral squamous cell carcinoma may play an important role in the carcinogenesis and progression of oral squamous cell carcinoma.