Interleukin-11 Increases Cell Motility and Up-Regulates Intercellular Adhesion Molecule-1 Expression in Human Chondrosarcoma Cells

被引:27
作者
Li, Te-Mao [2 ]
Wu, Chi-Ming [2 ]
Huang, Hsin-Chih [3 ]
Chou, Pei-Chi [2 ,4 ]
Fong, Yi-Chin [2 ,5 ]
Tang, Chih-Hsin [1 ,6 ]
机构
[1] China Med Univ, Dept Pharmacol, Sch Med, Taichung, Taiwan
[2] China Med Univ, Sch Chinese Med, Taichung, Taiwan
[3] Chi Mei Med Ctr, Tainan, Taiwan
[4] China Med Univ Hosp, Taipei Branch, Dept Chinese Med, Taipei, Taiwan
[5] China Med Univ Hosp, Dept Orthopaed, Taichung, Taiwan
[6] China Med Univ, Grad Inst Basic Med Sci, Taichung, Taiwan
关键词
IL-11; CHONDROSARCOMA; ICAM-1; MIGRATION; NF-KAPPA-B; GENE-EXPRESSION; ENDOTHELIAL-CELLS; SIGNALING PATHWAY; CARCINOMA CELLS; IL-11; RECEPTOR; CANCER CELLS; ACTIVATION; INVASION; ALPHA;
D O I
10.1002/jcb.24211
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Interleukin-11 (IL-11) was originally identified as the cytokine that could induce the proliferation of human cells. Recent studies have shown that IL-11 plays a critical role in tumor growth, angiogenesis, and metastasis. Chondrosarcoma is a type of highly malignant tumor with a potent capacity to invade locally and cause distant metastasis. However, the effects of IL-11 on human chondrosarcoma cells are largely unknown. Here, we found that IL-11 increased the migration and expression of intercellular adhesion molecule-1 (ICAM)-1 in human chondrosarcoma cells. We also found that human chondrosarcoma tissues had significant expression of the IL-11 which was higher than that in primary chondrocytes. The phosphatidylinositol 3-kinase (PI3K), Akt, and NF-?B pathways were activated by IL-11 treatment, and the IL-11-induced expression of ICAM-1 and migration activity were inhibited by the specific inhibitors and mutant forms of PI3K, Akt, and NF-?B cascades. Taken together, our results indicate that IL-11 enhanced the migration of the chondrosarcoma cells by increasing ICAM-1 expression through the IL-11Ra receptor, PI3K, Akt, and NF-?B signal transduction pathway. J. Cell. Biochem. 113: 33533362, 2012. (C) 2012 Wiley Periodicals, Inc.
引用
收藏
页码:3353 / 3362
页数:10
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