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Article Open Access

HIF‑1α‑induced upregulation of lncRNA UCA1 promotes cell growth in osteosarcoma by inactivating the PTEN/AKT signaling pathway

  • Authors:
    • Tengfei Li
    • Yang Xiao
    • Tunsheng Huang
  • View Affiliations / Copyright

    Affiliations: Department of Chinese and Western Μedicine Οrthopedics of 31 Ward, Loudi Central Hospital, Loudi, Hunan 417000, P.R. China
    Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1072-1080
    |
    Published online on: January 3, 2018
       https://doi.org/10.3892/or.2018.6182
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Abstract

Increasing evidence indicates that long non‑coding RNAs (lncRNAs) play an important role in multiple biological processes including cell growth, differentiation, proliferation and invasion. Urothelial carcinoma associated 1 (UCA1) is a highly conserved nuclear ncRNA and a key regulator of cell proliferation and apoptosis in several types of cancers. However, its role in osteosarcoma progression is not well known. In the present study, we aimed to determine the biological role of UCA1 in osteosarcoma progression. RT‑qPCR analysis showed that UCA1 expression was significantly increased in osteosarcoma cell lines and promoted cell growth in osteosarcoma. We then sought to determine the mechanism underlying the upregulation of UCA1 in osteosarcoma. Luciferase reporter assay and chromatin immunoprecipitation assay suggested that lncRNA UCA1 was induced by HIF‑1α and HIF‑1α interacts with the HIF‑1α response element in the promoter region of UCA1. In addition, the gain- and loss-of-functional assay showed that HIF‑1α promoted osteosarcoma cell growth through inducing the UCA1 expression level. More importantly, Cignal Signal Transduction Reporter Array and western blot assay showed that lncRNA UCA1 inactivated the PTEN/AKT signaling pathway. Finally, we observed that HIF‑1α induced cell growth through the UCA1/PTEN/AKT signaling pathway. To conclude, our integrated approach demonstrates that UCA1 confers a tumor promoter function by promoting cell proliferation and silencing of the PTEN/AKT signaling pathway in osteosarcoma. Thus, UCA1 can serve as a promising therapeutic target for osteosarcoma patients.
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Copy and paste a formatted citation
Spandidos Publications style
Li T, Xiao Y and Huang T: HIF‑1α‑induced upregulation of lncRNA UCA1 promotes cell growth in osteosarcoma by inactivating the PTEN/AKT signaling pathway. Oncol Rep 39: 1072-1080, 2018.
APA
Li, T., Xiao, Y., & Huang, T. (2018). HIF‑1α‑induced upregulation of lncRNA UCA1 promotes cell growth in osteosarcoma by inactivating the PTEN/AKT signaling pathway. Oncology Reports, 39, 1072-1080. https://doi.org/10.3892/or.2018.6182
MLA
Li, T., Xiao, Y., Huang, T."HIF‑1α‑induced upregulation of lncRNA UCA1 promotes cell growth in osteosarcoma by inactivating the PTEN/AKT signaling pathway". Oncology Reports 39.3 (2018): 1072-1080.
Chicago
Li, T., Xiao, Y., Huang, T."HIF‑1α‑induced upregulation of lncRNA UCA1 promotes cell growth in osteosarcoma by inactivating the PTEN/AKT signaling pathway". Oncology Reports 39, no. 3 (2018): 1072-1080. https://doi.org/10.3892/or.2018.6182
Copy and paste a formatted citation
x
Spandidos Publications style
Li T, Xiao Y and Huang T: HIF‑1α‑induced upregulation of lncRNA UCA1 promotes cell growth in osteosarcoma by inactivating the PTEN/AKT signaling pathway. Oncol Rep 39: 1072-1080, 2018.
APA
Li, T., Xiao, Y., & Huang, T. (2018). HIF‑1α‑induced upregulation of lncRNA UCA1 promotes cell growth in osteosarcoma by inactivating the PTEN/AKT signaling pathway. Oncology Reports, 39, 1072-1080. https://doi.org/10.3892/or.2018.6182
MLA
Li, T., Xiao, Y., Huang, T."HIF‑1α‑induced upregulation of lncRNA UCA1 promotes cell growth in osteosarcoma by inactivating the PTEN/AKT signaling pathway". Oncology Reports 39.3 (2018): 1072-1080.
Chicago
Li, T., Xiao, Y., Huang, T."HIF‑1α‑induced upregulation of lncRNA UCA1 promotes cell growth in osteosarcoma by inactivating the PTEN/AKT signaling pathway". Oncology Reports 39, no. 3 (2018): 1072-1080. https://doi.org/10.3892/or.2018.6182
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