海鞘醇衍生物SC002抗肿瘤相关分子机制的研究

Primary study on anti-tumor mechanisms of analog from SC002

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。

AIM： To study the anti-tumor mechanisms of ascidiacea analog SC002. METHODS： After treated the tumor cells with ascidiacea analog SC002, the changes of a serials of tumor associated cell signal molecules, including VEGF（vascular endothelial growth factor）, P53, P21 and Bcl-2 et al, were detected by Western blot; Further more, the expression of serum VEGF in tumor-bearing mice and the activity of Caspase-3, 8 , 9 in tumor tissue were investi- gated by ELISA; At last. RESULTS： Ascidiacea analog SC002 can obviously induce the expression of P53 , while decreasing the expression of Bcl-2 and VEGF, but have on effect on p21 in tumor tissue; ELISA shown that SC002 can also reduce the concentration of serum VEGF in tumor-bearing mice, but did not affected the activity of Caspase-3, 8 and 9. CONCLUSION： SC002 have the anti-tumor function through promoting the expression of tumor suppressor gene p53, suppress the expression of Bcl-2 and VEGF . This founding will provided an important base theory for it＇s further use as a novel anti-tumor drugs.