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目的:探讨多烯紫杉醇联合TNF-α抑制前列腺癌的作用,并进一步了解其作用机理。方法:建立人前列腺癌细胞的裸鼠皮下移植瘤模型,在多烯紫杉醇和TNF-α的联合作用下观察其对皮下移植瘤生长的抑制作用,并通过RT-PCR、免疫组化方法检测Bax、Bcl-2基因mRNA表达及p53蛋白表达。结果:与多烯紫杉醇组、TNF-α组及对照组相比,多烯紫杉醇和TNF-α联合治疗组可抑制前列腺癌皮下移植瘤生长速度,且肿瘤体积明显减少(P<0.01)。BaxmRNA表达上调,而Bcl-2mRNA表达水平下降,免疫组化结果表明p53蛋白的表达水平下降。结论:多烯紫杉醇联合TNF-α对前列腺癌有一定的抑制作用,作用机理可能是通过引起促凋亡基因Bax表达增高,从而导致肿瘤细胞加速凋亡而实现的。
Objective: To investigate the effect of docetaxel combined with TNF-α on prostate cancer and to further understand its mechanism. Methods: The subcutaneous xenograft model of human prostate cancer cells was established. The inhibitory effect of docetaxel and TNF-α on the growth of subcutaneous xenograft tumor was observed. The expression of Bax was detected by RT-PCR and immunohistochemistry , Bcl-2 mRNA expression and p53 protein expression. Results: Compared with docetaxel group, TNF-α group and control group, the combination of docetaxel and TNF-α could inhibit the growth of subcutaneous xenografts in prostate cancer and significantly reduce the tumor volume (P <0.01). The expression of Bax mRNA was up-regulated, but the expression of Bcl-2 mRNA was decreased. The expression of Bcl-2 mRNA was decreased by immunohistochemistry. CONCLUSION: Docetaxel combined with TNF-α can inhibit the proliferation of prostate cancer. The possible mechanism is that Paclitaxel combined with TNF-α can inhibit the apoptosis of tumor cells by inducing the increase of Bax expression.