Int J Oncol. 2015 Jan;46(1):185-94. doi: 10.3892/ijo.2014.2721. Epub 2014 Oct 22.
Silencing of galectin-3 represses osteosarcoma cell migration and invasion through inhibition of FAK/Src/Lyn activation and β-catenin expression and increases susceptibility to chemotherapeutic agents.
Park GB1, Kim DJ1, Kim YS1, Lee HK2, Kim CW3, Hur DY1.
Department of Anatomy and Research Center for Tumor Immunology, Inje University College of Medicine, Busan 614-735, Republic of Korea.
Department of Internal Medicine, Inje University Busan Paik Hospital, Busan 614-735, Republic of Korea.
Department of Orthopedic Surgery, Inje University Busan Paik Hospital, Busan 614-735, Republic of Korea.
Galectin-3 is involved in tumor cell proliferation, adhesion, angiogenesis and metastasis. Galectin-3 promotes β-catenin/Wnt signaling, and β-catenin-related oncogenesis has been frequently reported in osteosarcoma. However, the correlation between galectin-3 and β‑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 β-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.