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

TM Li, CM Wu, HC Huang, PC Chou… - Journal of cellular …, 2012 - Wiley Online Library
TM Li, CM Wu, HC Huang, PC Chou, YC Fong, CH Tang
Journal of cellular biochemistry, 2012Wiley Online Library
Abstract 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) …
Abstract
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‐κB 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‐κB cascades. Taken together, our results indicate that IL‐11 enhanced the migration of the chondrosarcoma cells by increasing ICAM‐1 expression through the IL‐11Rα receptor, PI3K, Akt, and NF‐κB signal transduction pathway. J. Cell. Biochem. 113: 3353–3362, 2012. © 2012 Wiley Periodicals, Inc.
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