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Downregulation of SOX3 leads to the inhibition of the proliferation, migration and invasion of osteosarcoma cells
Author(s) -
Yanjie Guo,
Jimin Yin,
Mingjie Tang,
Xingang Yu
Publication year - 2018
Publication title -
international journal of oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.405
H-Index - 122
ISSN - 1019-6439
DOI - 10.3892/ijo.2018.4278
Subject(s) - downregulation and upregulation , cell cycle , biology , osteosarcoma , oncogene , cancer research , cyclin d1 , cell growth , gene knockdown , proliferating cell nuclear antigen , carcinogenesis , microbiology and biotechnology , cell , apoptosis , cancer , biochemistry , genetics , gene
Sex determining region Y-box protein 3 (SOX3) is involved in embryonic development and tumorigenesis. However, the expression and precise role of SOX3 in osteosarcoma remain unclear. In this study, we reported that SOX3 expression was upregulated in osteosarcoma tissues compared with non-cancerous bone cyst tissues. To elucidate the cellular and molecular function of SOX3, we examined the consequences of SOX3 knockdown in osteosarcoma cells. We found that the downregulation of SOX3 inhibited the proliferation, migration and invasion of osteosarcoma cells. SOX3 downregulation also increased the cell population in the G1 phase and induced cell apoptosis. SOX3 knockdown-mediated cell cycle arrest and cell apoptosis were associated with decreased levels of Cdc25A, cyclin D1, proliferating cell nuclear antigen (PCNA) and Bcl-2, as well as an increased Bax expression. We also found that the downregulation of SOX3 decreased the expression of Snail, Twist and matrix metalloproteinase-9 (MMP-9), and increased E-cadherin expression, resulting in the inhibition of cell migration and invasion. Taken together, our data indicate that SOX3 may serve as an oncogene in osteosarcoma, and SOX3 downregulation may prove to be a novel approach for the inhibition of osteosarcoma progression.

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