期刊
INTERNATIONAL JOURNAL OF ONCOLOGY
卷 46, 期 1, 页码 185-194出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/ijo.2014.2721
关键词
galectin-3; FAK; Src; Lyn; beta-catenin; invasion; osteosarcoma
类别
资金
- Korea Drug Development Fund (KDDF) - Ministry of Science, ICT and Future Planning
- Ministry of Trade, Industry Energy
- Ministry of Health & Welfare (Republic of Korea) [KDDF-201404-04]
- National R&D Program for Cancer Control, Ministry for Health, Welfare and Family Affairs, Republic of Korea [0920040]
- Korea Evaluation Institute of Industrial Technology (KEIT) [KDDF-201404] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Galectin-3 is involved in tumor cell proliferation, adhesion, angiogenesis and metastasis. Galectin-3 promotes beta-catenin/Wnt signaling, and beta-catenin-related oncogenesis has been frequently reported in osteosarcoma. However, the correlation between galectin-3 and beta-catenin signaling in osteosarcoma is poorly defined. We hypothesized that galectin-3 may control the migration and invasion of cancer cells and that silencing of galectin-3 would therefore, suppress motility in osteosarcoma cells. In the present study, we show that galectin-3 silencing in cultured human osteosarcoma cells had decreased cell migration and invasion capabilities; reduced the expression and activation of FAK, Src, Lyn, PI3K/Akt, ERK1/2 and beta-catenin, which are key mediators of invasion; inhibited the expression and secretion of VEGF, MCP-1, IL-8, IL-6, MMP2/9 and phospho-Stat3; and potentiated sensitivity to cisplatin. Our results suggest that galectin-3 may be a feasible therapeutic target for osteosarcoma.
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