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      MicroRNA-132 inhibits cell growth and metastasis in osteosarcoma cell lines possibly by targeting Sox4

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          Abstract

          Increasing evidence has confirmed that dysregulation of microRNAs (miRNAs) can contribute to the progression and metastasis of human tumors. Previous studies have shown that dysregulation of microRNAs (miRNAs) can contribute to the progression and metastasis of human tumors. However, the precise mechanisms of miR-132 in osteosarcoma have not been well clarified. Real-time PCR was performed to detect the expression of miR-132 in osteosarcoma cell lines. miR-132 mimic, miR-132 inhibitor and negative control were transfected into osteosarcoma cells and the effects of miR-132 on the cell growth and metastasis were investigated. Furthermore, protein level of Sox4 was measured by western blotting. Luciferase assays were performed to validate Sox4 as miR-132 target in osteosarcoma cells. We found that miR-132 was downregulated in osteosarcoma cell lines. Introduction of miR-132 significantly inhibited proliferation, arrested cell cycle and induced apoptosis in osteosarcoma cells. Besides, invasion and epithelial-mesenchymal transition (EMT) of osteosarcoma cells was suppressed by overexpressing miR-132. However, downregulation of miR-132 promoted cell growth and metastasis in osteosarcoma cells. Bioinformatics analysis predicted that Sox4 was a potential target gene of miR-132. Luciferase reporter assay demonstrated that miR-132 could directly target Sox4. Moreover, the low level of miR-132 was associated with increased expression of Sox4 in osteosarcoma cells. Sox4 inhibition suppressed cell malignant behaviors. Overexpression of Sox4 in osteosarcoma cells transfected with miR-132 mimic partially reversed the inhibitory effect of miR-132. In conclusion, miR-132 inhibited cell growth and metastasis in osteosarcoma cells by downregulation of Sox4, and knockdown of Sox4 was essential for the miR-132-inhibited cell growth and metastasis in osteosarcoma cells.

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          Most cited references31

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          Cancer genes and the pathways they control.

          The revolution in cancer research can be summed up in a single sentence: cancer is, in essence, a genetic disease. In the last decade, many important genes responsible for the genesis of various cancers have been discovered, their mutations precisely identified, and the pathways through which they act characterized. The purposes of this review are to highlight examples of progress in these areas, indicate where knowledge is scarce and point out fertile grounds for future investigation.
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            The Rb/E2F pathway and cancer.

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            Over the past decade, studies focusing on the mechanisms controlling cellular proliferation have converged with equally intensive efforts directed at the analysis of oncogenic pathways associated with human cancer. These convergent studies have revealed the central role played by the pathway that controls the activity of the retinoblastoma tumor suppressor protein (Rb), which in turn regulates the E2F transcription factor. In particular, it is now clear that the Rb/E2F pathway is critical in regulating the initiation of DNA replication. It is also clear that the control of the pathway is disrupted in virtually all human cancers. Questions remain, however, as to the specific role played by individual activities within the pathway in the control of cell growth and their participation in the development of cancer.
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              Sex-determining region Y box 4 is a transforming oncogene in human prostate cancer cells.

              Prostate cancer is the most commonly diagnosed noncutaneous neoplasm and second most common cause of cancer-related mortality in western men. To investigate the mechanisms of prostate cancer development and progression, we did expression profiling of human prostate cancer and benign tissues. We show that the SOX4 is overexpressed in prostate tumor samples compared with benign tissues by microarray analysis, real-time PCR, and immunohistochemistry. We also show that SOX4 expression is highly correlated with Gleason score at the mRNA and protein level using tissue microarrays. Genes affected by SOX4 expression were also identified, including BCL10, CSF1, and NcoA4/ARA70. TLE-1 and BBC3/PUMA were identified as direct targets of SOX4. Silencing of SOX4 by small interfering RNA transfection induced apoptosis of prostate cancer cells, suggesting that SOX4 could be a therapeutic target for prostate cancer. Stable transfection of SOX4 into nontransformed prostate cells enabled colony formation in soft agar, suggesting that, in the proper cellular context, SOX4 can be a transforming oncogene.
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                Author and article information

                Journal
                Int J Oncol
                Int. J. Oncol
                IJO
                International Journal of Oncology
                D.A. Spandidos
                1019-6439
                1791-2423
                November 2015
                07 September 2015
                07 September 2015
                : 47
                : 5
                : 1672-1684
                Affiliations
                Department of Orthopaedic Surgery, China-Japan Union Hospital of Jilin University, Changchun 130031, P.R. China
                Author notes
                Correspondence to: Dr Qingsan Zhu, Department of Orthopaedic Surgery, China-Japan Union Hospital of Jilin University, 126 Xiantai Street, Changchun 130033, P.R. China, E-mail: zhuqingsan2010@ 123456yeah.net
                Article
                ijo-47-05-1672
                10.3892/ijo.2015.3147
                4599193
                26352673
                79534fe7-0dfc-4507-ac96-cbeaf1b2d0bb
                Copyright: © Liu et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 20 June 2015
                : 07 August 2015
                Categories
                Articles

                mir-132,osteosarcoma,sox4,proliferation,invasion,epithelial-mesenchymal transition

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