Jia Li, Xu Henggui, Zhao Yongfu, Jiang Lili, Yu Jingda, Zhang Jianing
Department of Biochemistry, Institute of Glycobiology, Dalian Medical University, Dalian, China.
Cancer Invest. 2008 Dec;26(10):977-83. doi: 10.1080/07357900802072723.
Multidrug resistant (MDR) tumor cells over-expressing P-glycoprotein exhibit variation in invasive behavior. To investigate the mechanisms, we analyzed the expression of CD147. The results showed that CD147 expression was increased in HepG2/Adr cells, as compared to HepG2 cells. The MDR cells produced more MMP11 and MDR1, which promoted HepG2/Adr cells invasion and increased resistance to chemotherapeutic drugs. On the other hand, CD147 silencing in HepG2/Adr cells by RNAi led to the opposite effect. Treatment of tumor cells with U-0126, an inhibitor of MAPK/Erk, also down-regulated MMP11 and MDR1 expression. Thus, CD147 may functionally mediate tumor cells invasion and MDR.
过表达P-糖蛋白的多药耐药（MDR）肿瘤细胞在侵袭行为上表现出差异。为了研究其机制，我们分析了CD147的表达。结果显示，与HepG2细胞相比，HepG2/Adr细胞中CD147的表达增加。MDR细胞产生更多的MMP11和MDR1，这促进了HepG2/Adr细胞的侵袭并增加了对化疗药物的耐药性。另一方面，通过RNAi使HepG2/Adr细胞中的CD147沉默则产生相反的效果。用MAPK/Erk抑制剂U-0126处理肿瘤细胞也下调了MMP11和MDR1的表达。因此，CD147可能在功能上介导肿瘤细胞的侵袭和多药耐药。
