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CD147的表达介导了肝癌细胞的侵袭和多药耐药性。

Expression of CD147 mediates tumor cells invasion and multidrug resistance in hepatocellular carcinoma.

作者信息

Jia Li, Xu Henggui, Zhao Yongfu, Jiang Lili, Yu Jingda, Zhang Jianing

机构信息

Department of Biochemistry, Institute of Glycobiology, Dalian Medical University, Dalian, China.

出版信息

Cancer Invest. 2008 Dec;26(10):977-83. doi: 10.1080/07357900802072723.

Abstract

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.

摘要

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。

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