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目的:探讨海鞘醇衍生物002(简称SC002)抗肿瘤相关分子机制。方法:应用Western blot检测SC002作用于肿瘤细胞后,VEGF、P53、P21、Bcl-2等肿瘤相关信号分子表达水平的变化;进一步应用ELISA检测SC002对荷瘤小鼠血清中的VEGF和实体瘤组织中Caspase-3,8,9活性的影响。结果:SC002可明显诱导P53的表达,而降低BCL-2的表达,但对p21没有作用;SC002可降低荷瘤小鼠血清中VEGF的含量,同时对瘤体组织中VEGF蛋白表达水平也有抑制作用,但对Caspase-3,8,9的活性无明显影响。结论:SC002可通过激活抑癌基因p53,抑制抗凋亡基因Bcl-2和促血管生成因子VEGF等多种途径,发挥抗肿瘤的活性,这一发现将为SC002作为新型的抗肿瘤药物提供重要的实验依据。
Objective: To investigate the anti-tumor related molecular mechanism of the sarcitol derivative 002 (referred to as SC002). Methods: The expression of VEGF, P53, P21, Bcl-2 and other tumor-related signal molecules in SC002 cells were detected by Western blot. The expression of VEGF and tumor tissue in SCLC mice was detected by ELISA Caspase-3,8,9 activity. Results: SC002 could obviously induce the expression of P53 and decrease the expression of BCL-2, but had no effect on p21. SC002 could reduce the content of VEGF in the tumor-bearing mice and inhibit the expression of VEGF protein in tumor tissues , But no significant effect on the activity of Caspase-3,8,9. Conclusion: SC002 can exert anti-tumor activity by activating the tumor suppressor gene p53, inhibiting the anti-apoptotic gene Bcl-2 and pro-angiogenic factor VEGF, and this finding will provide important evidence for SC002 as a novel anti-tumor drug Experimental basis.