CTGF increases matrix metalloproteinases expression and subsequently promotes tumor metastasis in human osteosarcoma through down-regulating miR-519d

ASIA unversity > 醫學暨健康學院 > 生物科技學系 > 期刊論文 > Item 310904400/81131

Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/81131

Title:	CTGF increases matrix metalloproteinases expression and subsequently promotes tumor metastasis in human osteosarcoma through down-regulating miR-519d
Authors:	Ts, Hsiao-Chi;Tsai, Hsiao-Chi;Su, Hong-Lin;Su, Hong-Lin;Hua, Chun-Yin;Huang, Chun-Yin;Fong, Yi-Chin;Fong, Yi-Chin;Hs, Chin-Jung;Hsu, Chin-Jung;湯智昕;Chih-Hsin, Tang;*
Contributors:	生物科技學系
Date:	2014-06
Issue Date:	2014-10-01 08:32:16 (UTC+0)
Abstract:	Osteosarcoma, the most common primary malignant bone tumor, shows potent capacity for local invasion and distant metastasis. Connective tissue growth factor (CTGF/CCN2), a secreted protein, binds to integrins, modulates invasive behavior of certain human cancer cells. Effect of CTGF in metastasis of human osteosarcoma is unknown. We found overexpression of CTGF increasing matrix metalloproteinases (MMPs)-2 and MMP-3 expression as well as promoting cell migration. MicroRNA (miRNA) analysis of CTGF-overexpressed osteosarcoma versus control cells probed mechanisms of CTGF-mediated promotion of migration. Among miRNAs regulated by CTGF, miR-519d was most downregulated after CTGF treatment. Co-transfection with miR-519d mimic reversed CTGF-mediated MMPs expression and cell migration. Also, MEK and ERK inhibitors or mutants reduced CTGF-increased cell migration and miR-519d suppression. By contrast, knockdown of CTGF diminished lung metastasis in vivo. Clinical samples indicate CTGF expression as linked with clinical stage and tumor metastasis. Taken together, data show CTGF elevating MMPs expression and subsequently promoting tumor metastasis in human osteosarcoma, down-regulating miR-519d via MEK and ERK pathways, making CTGF a new molecular therapeutic target in osteosarcoma metastasis.
Relation:	Oncotarget;5(11):3800-12.
Appears in Collections:	[生物科技學系] 期刊論文

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