Silencing CD147 inhibits tumor progression and increases chemosensitivity in murine lymphoid neoplasm P388D1 cells

被引:24
作者
Jia, Li [1 ,2 ]
Wei, Wei [2 ]
Cao, Jun [3 ]
Xu, Henggui [2 ]
Miao, Xiaoyan [2 ]
Zhang, Jianing [1 ]
机构
[1] Dalian Med Univ, Dept Biochem, Inst Glycobiol, Dalian 116044, Liaoning Prov, Peoples R China
[2] Dalian Med Univ, Coll Lab Med, Dalian 116044, Liaoning Prov, Peoples R China
[3] Dalian Med Univ, Dept Toxicol, Dalian 116044, Liaoning Prov, Peoples R China
基金
中国国家自然科学基金;
关键词
CD147; RNA interference; P388D1; cells; Tumor progression; MATRIX-METALLOPROTEINASE INDUCER; CANCER-CELLS; MULTIDRUG-RESISTANCE; PROTEIN-KINASES; GROWTH-FACTOR; HCA-F; EXPRESSION; INVASION; MAPK; MMP;
D O I
10.1007/s00277-008-0678-2
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Overexpression of extracellular matrix metalloproteinase inducer (EMMPRIN or CD147), a member glycoprotein enriched on the surface of many malignant tumor cells, promotes tumor progression and confers resistance to some chemotherapeutic drugs. To investigate the possible role of CD147 in the macrophage-like lymphoid neoplasm P388D1 cells progression, we used RNA interference approach to silence CD147 expression. The results showed that silencing of CD147 in P388D1 cells impeded the expression of MMP11 at both mRNA and protein levels. The reduced CD147 expression also resulted in reductions in tumorigenicity, as well as decreased in regional lymph node metastasis. Furthermore, the down-regulation of CD147 expression sensitized cells to be more sensitive to chemotherapeutic drugs. Treatment of tumor cells with U-0126, an inhibitor of mitogen-activated protein kinase/Erk, also down-regulated the expression of MMP11. Our current results indicate that the expression of CD147 functionally mediates tumor progression and is a potential target for therapeutic anti-cancer drugs.
引用
收藏
页码:753 / 760
页数:8
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