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November 2012 Volume 28 Issue 5

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Article

miR-15a and miR-16-1 downregulate CCND1 and induce apoptosis and cell cycle arrest in osteosarcoma

  • Authors:
    • Cheng-Kui Cai
    • Guang-Yi Zhao
    • Li-Ying Tian
    • Lie Liu
    • Kang Yan
    • Yun-Lei Ma
    • Zhen-Wei Ji
    • Xiao-Xiang Li
    • Kang Han
    • Jie Gao
    • Xiu-Chun Qiu
    • Qing-Yu Fan
    • Tong-Tao Yang
    • Bao-An Ma
  • View Affiliations / Copyright

    Affiliations: Department of Orthopedic Surgery Center and Orthopedic Oncology Institute of People's Liberation Army, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China , Department of Orthopedics, Baoji Center Hospital, Baoji, Shaanxi 710038, P.R. China
  • Pages: 1764-1770
    |
    Published online on: August 24, 2012
       https://doi.org/10.3892/or.2012.1995
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Abstract

Osteosarcoma, the most common primary tumor of the bones, causes many deaths due to its rapid proliferation and drug resistance. Recent studies have shown that cyclin D1 plays a key regulatory role during cell proliferation, and non-coding microRNAs (miRNAs) act as crucial modulators of cyclin D1 (CCND1). The aim of the current study was to determine the role of miRNAs in controlling CCND1 expression and inducing cell apoptosis. CCND1 has been found to be a target of miR-15a and miR-16-1 through analysis of complementary sequences between microRNAs and CCND1 mRNA. The upregulation of miR-15a and miR-16-1 in the cell line SOSP-9607 induces apoptosis and cell cycle arrest. Osteosarcoma cells transfected with miR-15a and miR-16-1 show slower proliferation curves. Moreover, the transcription of CCND1 is suppressed by miR-15a and miR-16-1 via direct binding to the CCND1 3'-untranslated region (3'-UTR). The data presented here demonstrate that the CCND1 contributes to osteosarcoma cell proliferation, suggesting that repression of CCND1 by miR-15a and miR-16-1 could be used for osteosarcoma therapy.
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Copy and paste a formatted citation
Spandidos Publications style
Cai C, Zhao G, Tian L, Liu L, Yan K, Ma Y, Ji Z, Li X, Han K, Gao J, Gao J, et al: miR-15a and miR-16-1 downregulate CCND1 and induce apoptosis and cell cycle arrest in osteosarcoma. Oncol Rep 28: 1764-1770, 2012.
APA
Cai, C., Zhao, G., Tian, L., Liu, L., Yan, K., Ma, Y. ... Ma, B. (2012). miR-15a and miR-16-1 downregulate CCND1 and induce apoptosis and cell cycle arrest in osteosarcoma. Oncology Reports, 28, 1764-1770. https://doi.org/10.3892/or.2012.1995
MLA
Cai, C., Zhao, G., Tian, L., Liu, L., Yan, K., Ma, Y., Ji, Z., Li, X., Han, K., Gao, J., Qiu, X., Fan, Q., Yang, T., Ma, B."miR-15a and miR-16-1 downregulate CCND1 and induce apoptosis and cell cycle arrest in osteosarcoma". Oncology Reports 28.5 (2012): 1764-1770.
Chicago
Cai, C., Zhao, G., Tian, L., Liu, L., Yan, K., Ma, Y., Ji, Z., Li, X., Han, K., Gao, J., Qiu, X., Fan, Q., Yang, T., Ma, B."miR-15a and miR-16-1 downregulate CCND1 and induce apoptosis and cell cycle arrest in osteosarcoma". Oncology Reports 28, no. 5 (2012): 1764-1770. https://doi.org/10.3892/or.2012.1995
Copy and paste a formatted citation
x
Spandidos Publications style
Cai C, Zhao G, Tian L, Liu L, Yan K, Ma Y, Ji Z, Li X, Han K, Gao J, Gao J, et al: miR-15a and miR-16-1 downregulate CCND1 and induce apoptosis and cell cycle arrest in osteosarcoma. Oncol Rep 28: 1764-1770, 2012.
APA
Cai, C., Zhao, G., Tian, L., Liu, L., Yan, K., Ma, Y. ... Ma, B. (2012). miR-15a and miR-16-1 downregulate CCND1 and induce apoptosis and cell cycle arrest in osteosarcoma. Oncology Reports, 28, 1764-1770. https://doi.org/10.3892/or.2012.1995
MLA
Cai, C., Zhao, G., Tian, L., Liu, L., Yan, K., Ma, Y., Ji, Z., Li, X., Han, K., Gao, J., Qiu, X., Fan, Q., Yang, T., Ma, B."miR-15a and miR-16-1 downregulate CCND1 and induce apoptosis and cell cycle arrest in osteosarcoma". Oncology Reports 28.5 (2012): 1764-1770.
Chicago
Cai, C., Zhao, G., Tian, L., Liu, L., Yan, K., Ma, Y., Ji, Z., Li, X., Han, K., Gao, J., Qiu, X., Fan, Q., Yang, T., Ma, B."miR-15a and miR-16-1 downregulate CCND1 and induce apoptosis and cell cycle arrest in osteosarcoma". Oncology Reports 28, no. 5 (2012): 1764-1770. https://doi.org/10.3892/or.2012.1995
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