National Changhua University of Education Institutional Repository : Item 987654321/17854

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NCUEIR > College of Social Science and Physical Education > sh > Periodical Articles > Item 987654321/17854

Please use this identifier to cite or link to this item: http://ir.ncue.edu.tw/ir/handle/987654321/17854

Title:	Leptin Enhances Cell Migration in Human Chondrosarcoma Cells through OBRl Leptin Receptor
Authors:	Yang, Shu-Ning;Chuang, Jing-Yuan;Fong, Yi-Chin;Chen, Hsien-Te;Huan, Chun-Yiu;Yang, Wei-Hung;Su, Chen-Ming;Tseng, Wen-Pei;Tang, Chih-Hsin
Contributors:	運動健康所
Date:	2009-04
Issue Date:	2014-01-15T04:02:50Z
Publisher:	Oxford University Press
Abstract:	Leptin, an adipocyte-derived cytokine that is closely associated with obesity, has recently been shown to be involved in carcinogenesis and cancer progression. Integrins are the major adhesive molecules in mammalian cells and have been associated with metastasis of cancer cells. In this study, we found that leptin increased the migration and the expression of αvβ3 integrin in human chondrosarcoma cells. We also found that human chondrosarcoma tissues and chondrosarcoma cell lines had significant expression of the long form (OBRl) leptin receptor, which was higher than that in normal cartilage and human primary chondrocyte. Leptin-mediated migration and integrin upregulation were attenuated by OBRl receptor antisense oligonucleotide. Activations of insulin receptor substrate (IRS)-1, phosphatidylinositol 3-kinase (PI3K), Akt and nuclear factor-κB (NF-κB) pathways after leptin treatment were demonstrated, and leptin-induced expression of integrin and migration activity was inhibited by the specific inhibitor, small-interfering RNA and mutant of IRS-1, PI3K, Akt and NF-κB cascades. Taken together, our results indicated that leptin enhances the migration of chondrosarcoma cells by increasing αvβ3 integrin expression through the OBR1/IRS-1/PI3K/Akt/NF-κB signal transduction pathway.
Relation:	Carcinogenesis, 30(4): 566-574
Appears in Collections:	[sh] Periodical Articles

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