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Silencing of histone methyltransferase NSD3 reduces cell viability in osteosarcoma with induction of apoptosis

  • Authors:
    • Zhiwei Liu
    • Lianhua Piao
    • Ming Zhuang
    • Xubin Qiu
    • Xiaoshuang Xu
    • Dawei Zhang
    • Mengmeng Liu
    • Ding Ren
  • View Affiliations / Copyright

    Affiliations: Department of Orthopaedics, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu 213000, P.R. China, Institute of Bioinformatics and Medical Engineering, Jiangsu University of Technology, Changzhou, Jiangsu 213001, P.R. China, Out-Patient Department, PLA No. 85th Hospital, Shanghai 200006, P.R. China
    Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2796-2802
    |
    Published online on: September 4, 2017
       https://doi.org/10.3892/or.2017.5936
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Abstract

NSD3 is a histone lysine methyltransferase that methylates histone H3 at lysine 36. NSD3 is located at chromosome 8p11.23, the locus that exhibits strong cancer relevance. Thus, NSD3 is likely involved in multiple human cancers. Nevertheless, its roles in human carcinogenesis remain unknown. In the present study, we demonstrated that silencing of NSD3 in osteosarcoma, the most common primary bone cancer in children and adolescents, results in a marked decrease in the number of viable cancer cells, accompanied by increases in the cell population at the G2/M phase and the number of apoptotic cells. In addition, 549 NSD3‑regulated genes were identified and a set of selected candidate genes were validated. Bioinformatic analysis revealed that NSD3 negatively regulates a number of genes that are involved in the process of negative regulation of signal transduction as well as negative regulation of signaling and cell communication. Our results indicate the oncogenic roles of NSD3 in the development and progression of human osteosarcoma, and implicate NSD3 as a potential molecular target for selective therapy for human osteosarcoma.
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Copy and paste a formatted citation
Spandidos Publications style
Liu Z, Piao L, Zhuang M, Qiu X, Xu X, Zhang D, Liu M and Ren D: Silencing of histone methyltransferase NSD3 reduces cell viability in osteosarcoma with induction of apoptosis. Oncol Rep 38: 2796-2802, 2017.
APA
Liu, Z., Piao, L., Zhuang, M., Qiu, X., Xu, X., Zhang, D. ... Ren, D. (2017). Silencing of histone methyltransferase NSD3 reduces cell viability in osteosarcoma with induction of apoptosis. Oncology Reports, 38, 2796-2802. https://doi.org/10.3892/or.2017.5936
MLA
Liu, Z., Piao, L., Zhuang, M., Qiu, X., Xu, X., Zhang, D., Liu, M., Ren, D."Silencing of histone methyltransferase NSD3 reduces cell viability in osteosarcoma with induction of apoptosis". Oncology Reports 38.5 (2017): 2796-2802.
Chicago
Liu, Z., Piao, L., Zhuang, M., Qiu, X., Xu, X., Zhang, D., Liu, M., Ren, D."Silencing of histone methyltransferase NSD3 reduces cell viability in osteosarcoma with induction of apoptosis". Oncology Reports 38, no. 5 (2017): 2796-2802. https://doi.org/10.3892/or.2017.5936
Copy and paste a formatted citation
x
Spandidos Publications style
Liu Z, Piao L, Zhuang M, Qiu X, Xu X, Zhang D, Liu M and Ren D: Silencing of histone methyltransferase NSD3 reduces cell viability in osteosarcoma with induction of apoptosis. Oncol Rep 38: 2796-2802, 2017.
APA
Liu, Z., Piao, L., Zhuang, M., Qiu, X., Xu, X., Zhang, D. ... Ren, D. (2017). Silencing of histone methyltransferase NSD3 reduces cell viability in osteosarcoma with induction of apoptosis. Oncology Reports, 38, 2796-2802. https://doi.org/10.3892/or.2017.5936
MLA
Liu, Z., Piao, L., Zhuang, M., Qiu, X., Xu, X., Zhang, D., Liu, M., Ren, D."Silencing of histone methyltransferase NSD3 reduces cell viability in osteosarcoma with induction of apoptosis". Oncology Reports 38.5 (2017): 2796-2802.
Chicago
Liu, Z., Piao, L., Zhuang, M., Qiu, X., Xu, X., Zhang, D., Liu, M., Ren, D."Silencing of histone methyltransferase NSD3 reduces cell viability in osteosarcoma with induction of apoptosis". Oncology Reports 38, no. 5 (2017): 2796-2802. https://doi.org/10.3892/or.2017.5936
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