RANKL Increases Migration of Human Lung Cancer Cells Through Intercellular Adhesion Molecule-1 Up-Regulation

ASIA unversity > 醫學暨健康學院 > 生物科技學系 > 期刊論文 > Item 310904400/16204

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題名:	RANKL Increases Migration of Human Lung Cancer Cells Through Intercellular Adhesion Molecule-1 Up-Regulation
作者:	黃志揚;HUANG, CHIH-YANG
貢獻者:	生物科技學系
關鍵詞:	RANKL;RANK;migration;lung cancer;ERK
日期:	2011
上傳時間:	2012-11-23 09:09:53 (UTC+0)
摘要:	Invasion of distant tissues by tumor cells is the primary cause of therapeutic failure in the treatment of malignant lung cancer cells. Receptor activator of nuclear factor-κB ligand (RANKL) and its receptor, RANK, play a key role in osteoclastogenesis and tumor metastasis. Intercellular adhesion molecule-1 (ICAM-1, also called CD54), a member of the immunoglobulin supergene family, is an inducible surface glycoprotein that mediates adhesion-dependent cell-to-cell interactions. The effects of RANKL on cell migration and ICAM-1 expression in human lung cancer cells are largely unknown. We found that RANKL directed the migration and increased ICAM-1 expression in human lung cancer (A549) cells. Pretreatment of A549 cells with the MAPK kinase (MEK) inhibitor PD98059 or U0126 inhibited RANKL-mediated migration and ICAM-1 expression. Stimulation of cells with RANKL increased the phosphorylation of MEK and extracellular signal-regulating kinase (ERK). In addition, an NF-κB inhibitor (PDTC) and IκB protease inhibitor (TPCK) also inhibited RANKL-mediated cell migration and ICAM-1 up-regulation. Taken together, these results suggest that the RANKL and RANK interaction acts through MEK/ERK, which in turn activates NF-κB, resulting in the activation of ICAM-1 and contributing to the migration of human lung cancer cells.
關聯:	JOURNAL OF CELLULAR BIOCHEMISTRY
顯示於類別:	[生物科技學系] 期刊論文

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