机构地区: 重庆大学生物医学工程联合学院
出 处: 《生命科学研究》 2010年第2期100-105,共6页
摘 要: 通过体外考察CXCR7(chemokine(C-X-Cmotif)receptor 7)在肝癌细胞中的表达和CXCR7抗体阻断后对肝癌细胞增殖、迁移、黏附等过程的影响,初步探讨CXCR7对肝癌细胞生物学特性的影响及作为肝癌治疗靶标的可能性.用Reverse transcription-PCR和Western-blot免疫印迹法检测HepG2细胞中CXCR4(chemokine(C-X-C motif)receptor4)和CXCR7的表达情况;用MTT法测定分别用抗体阻断CXCR4、CXCR7后,对HepG2细胞增殖率的影响;通过transwel小室体外侵袭迁移实验检测anti-CXCR4和anti-CXCR7对HepG2细胞趋化活性的影响.用CXCR4和CXCR7抗体分别预处理HepG2细胞后,考察其与单层HUVEC细胞黏附作用.结果表明HepG2细胞中都表达CXCR4和CXCR7这两个受体.用CXCR7抗体封闭后,HepG2细胞的增殖活力显著下降.CXCR7抗体对SDF-1诱导的HepG2细胞迁移影响不显著.CXCR4与CXCR7抗体都会抑制HepG2细胞与HUVEC细胞单层的黏附,CXCR7抗体抑制效果更明显.SDF-1对肝癌细胞的增殖、迁移、黏附有直接的促进作用,CXCR7在其中起着与CXCR4不完全相同但相互协同的重要作用.抗体阻断CXCR7能够抑制肝癌细胞的增殖、迁移、粘附,表明CXCR7有作为肝癌治疗靶标的潜力. To explore the expression of CXCR7 on hepatoma cells and the effect of CXCR7 on the proliferation, migration, and adhesion of the hepatoma cells in vitro. To preliminary study CXCR7 on the characteristics of hepatoma cell biology and therapeutic targets, as the possibility of liver cancer. The expression of CXCR4 and CXCR7 on HepG2 cells was detected with Reverse transcription-PCR and Western-blot. Proliferation of the HepG2 cells was detected by MTT, after they were blocked by anti- CXCR4, anti-CXCR7 respectively. The effect of anti-CXCR4 and anti-CXCR7 respectively on the chemotaxis of the hepatoma cells were detected by transwell chamber chemotaxis experiments. By the treatment of the anti-CXCR4, anti-CXCR7, to explore the adhesion of HepG2 cells on the HUVEC. The concentrations of CXCR4 and CXCR7 were expressed on HepG2 cells. Anti -CXCR7 abolished significantly the effects induced by CXCR7 on proliferation. The CXCR7 was no significant rele in the migration of HepG2 cells. Both of anti-CXCR4 and anti-CXCB7 impacted on the adhesion of HepG2 cells in vitro, however, the anti-CXCR7 was more pronounced inhibitory effect than the anti-CXCR4. It is concluded that the SDF-1 plays a direct promoting role in proliferation, migration, and adhesion of the hepatoma cells. CXCR7 plays a different but synergistic role as compared with that of CXCR4. Anti-CXCR7 possibly abolished the induction, so that it is potential as a therapy target for liver cancer.