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Homeobox B3 promotes tumor cell proliferation and invasion in glioblastoma

  • Authors:
    • Ke Xu
    • Chun Qiu
    • Hua Pei
    • Muhammad Aamer Mehmood
    • Huamin Wang
    • Liang Li
    • Qianfeng Xia
  • View Affiliations / Copyright

    Affiliations: Department of Immunology, School of Tropical and Laboratory Medicine, Hainan Medical University, Haikou, Hainan 571101, P.R. China, Department of Oncology, Hainan Provincial People's Hospital, Haikou, Hainan 571101, P.R. China, Department of Bioinformatics and Biotechnology, Government College University Faisalabad, Faisalabad, Punjab 38000, Pakistan, Key Laboratory of Tropical Biomedicine, and Faculty of Tropical Medicine and Laboratory Medicine, Hainan Medical University, Haikou, Hainan 571101, P.R. China
    Copyright: © Xu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 3712-3718
    |
    Published online on: January 8, 2018
       https://doi.org/10.3892/ol.2018.7750
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Abstract

Glioblastoma (GBM) is the most aggressive brain tumor in adults with the highest mortality rate. Despite advances achieved in treatment and research, the median survival for patients with GBM remains <1.5 years. This figure prompted the present study to identify novel genes associated with GBM development and progression to ultimately improve GBM treatment. The current study sought to determine the role of homeobox B3 (HOXB3) in GBM cell invasion and proliferation. HOXB3 was highly expressed in GBM tissues and glioma cell lines. To establish in vitro cell models for investigation, U87‑MG and U251‑MG, two typical GBM cells, were selected to generate corresponding cells lines that constitutively silenced HOXB3 expression using a lentivirus‑mediated RNA interference approach. The results of the knockdown revealed that glioma cells stably expressing HOXB3 short hairpin RNA exhibited significantly decreased proliferation levels when compared with untransfected cells. The effect of HOXB3 on glioma cell invasion was also examined. Silencing of HOXB3 resulted in a marked reduction in invasiveness. Furthermore, HOXB3 silencing led to the upregulation of E‑cadherin and downregulation of mesenchymal markers, N‑cadherin and vimentin. Taken together, the findings of the present study indicate that HOXB3 promotes cell proliferation and invasion.
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Copy and paste a formatted citation
Spandidos Publications style
Xu K, Qiu C, Pei H, Mehmood MA, Wang H, Li L and Xia Q: Homeobox B3 promotes tumor cell proliferation and invasion in glioblastoma. Oncol Lett 15: 3712-3718, 2018.
APA
Xu, K., Qiu, C., Pei, H., Mehmood, M.A., Wang, H., Li, L., & Xia, Q. (2018). Homeobox B3 promotes tumor cell proliferation and invasion in glioblastoma. Oncology Letters, 15, 3712-3718. https://doi.org/10.3892/ol.2018.7750
MLA
Xu, K., Qiu, C., Pei, H., Mehmood, M. A., Wang, H., Li, L., Xia, Q."Homeobox B3 promotes tumor cell proliferation and invasion in glioblastoma". Oncology Letters 15.3 (2018): 3712-3718.
Chicago
Xu, K., Qiu, C., Pei, H., Mehmood, M. A., Wang, H., Li, L., Xia, Q."Homeobox B3 promotes tumor cell proliferation and invasion in glioblastoma". Oncology Letters 15, no. 3 (2018): 3712-3718. https://doi.org/10.3892/ol.2018.7750
Copy and paste a formatted citation
x
Spandidos Publications style
Xu K, Qiu C, Pei H, Mehmood MA, Wang H, Li L and Xia Q: Homeobox B3 promotes tumor cell proliferation and invasion in glioblastoma. Oncol Lett 15: 3712-3718, 2018.
APA
Xu, K., Qiu, C., Pei, H., Mehmood, M.A., Wang, H., Li, L., & Xia, Q. (2018). Homeobox B3 promotes tumor cell proliferation and invasion in glioblastoma. Oncology Letters, 15, 3712-3718. https://doi.org/10.3892/ol.2018.7750
MLA
Xu, K., Qiu, C., Pei, H., Mehmood, M. A., Wang, H., Li, L., Xia, Q."Homeobox B3 promotes tumor cell proliferation and invasion in glioblastoma". Oncology Letters 15.3 (2018): 3712-3718.
Chicago
Xu, K., Qiu, C., Pei, H., Mehmood, M. A., Wang, H., Li, L., Xia, Q."Homeobox B3 promotes tumor cell proliferation and invasion in glioblastoma". Oncology Letters 15, no. 3 (2018): 3712-3718. https://doi.org/10.3892/ol.2018.7750
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