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Article Open Access

Hypoxia exposure upregulates MALAT‑1 and regulates the transcriptional activity of PTB‑associated splicing factor in A549 lung adenocarcinoma cells

  • Authors:
    • Ling Hu
    • Jing Tang
    • Xiaohuan Huang
    • Tao Zhang
    • Xiaoling Feng
  • View Affiliations / Copyright

    Affiliations: Department of Pathology, Chongqing Three Gorges Medical College, Chongqing 400000, P.R. China
    Copyright: © Hu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 294-300
    |
    Published online on: May 4, 2018
       https://doi.org/10.3892/ol.2018.8637
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Abstract

Hypoxia has been reported to be a critical microenvironmental factor that induces cancer metastasis and proliferation in gastric, liver and hepatic cancers; however, the underlying mechanisms of this are largely unknown. Long noncoding RNAs (lncRNAs) have emerged as crucial factors of several aspects of tumor malignancy, including tumorigenesis, metastasis and chemoresistance. However, the potential association of lncRNAs with hypoxia‑induced cancer malignancy remains to be determined. In the present study, the differential expression of lncRNAs following the induction of hypoxia in A549 lung adenocarcinoma cells was analyzed reverse transcription‑quantitative polymerase chain reaction. It was identified that the lncRNA metastasis‑associated lung adenocarcinoma transcript‑1 (MALAT‑1) was upregulated significantly by hypoxia in A549 cells. By considering its promotive effects on malignant tumor behaviors, in the present study, it was identified that upregulated MALAT‑1 released the binding of PTB‑associated splicing factor (PSF) to its target gene, GAGE6, and thus promoted proliferation, migration and invasion of A549 cells following hypoxia exposure. These results advance the overall understanding of the mechanism of hypoxia‑induced lung cancer metastasis and may assist in the development of novel therapeutics.
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Copy and paste a formatted citation
Spandidos Publications style
Hu L, Tang J, Huang X, Zhang T and Feng X: Hypoxia exposure upregulates MALAT‑1 and regulates the transcriptional activity of PTB‑associated splicing factor in A549 lung adenocarcinoma cells. Oncol Lett 16: 294-300, 2018.
APA
Hu, L., Tang, J., Huang, X., Zhang, T., & Feng, X. (2018). Hypoxia exposure upregulates MALAT‑1 and regulates the transcriptional activity of PTB‑associated splicing factor in A549 lung adenocarcinoma cells. Oncology Letters, 16, 294-300. https://doi.org/10.3892/ol.2018.8637
MLA
Hu, L., Tang, J., Huang, X., Zhang, T., Feng, X."Hypoxia exposure upregulates MALAT‑1 and regulates the transcriptional activity of PTB‑associated splicing factor in A549 lung adenocarcinoma cells". Oncology Letters 16.1 (2018): 294-300.
Chicago
Hu, L., Tang, J., Huang, X., Zhang, T., Feng, X."Hypoxia exposure upregulates MALAT‑1 and regulates the transcriptional activity of PTB‑associated splicing factor in A549 lung adenocarcinoma cells". Oncology Letters 16, no. 1 (2018): 294-300. https://doi.org/10.3892/ol.2018.8637
Copy and paste a formatted citation
x
Spandidos Publications style
Hu L, Tang J, Huang X, Zhang T and Feng X: Hypoxia exposure upregulates MALAT‑1 and regulates the transcriptional activity of PTB‑associated splicing factor in A549 lung adenocarcinoma cells. Oncol Lett 16: 294-300, 2018.
APA
Hu, L., Tang, J., Huang, X., Zhang, T., & Feng, X. (2018). Hypoxia exposure upregulates MALAT‑1 and regulates the transcriptional activity of PTB‑associated splicing factor in A549 lung adenocarcinoma cells. Oncology Letters, 16, 294-300. https://doi.org/10.3892/ol.2018.8637
MLA
Hu, L., Tang, J., Huang, X., Zhang, T., Feng, X."Hypoxia exposure upregulates MALAT‑1 and regulates the transcriptional activity of PTB‑associated splicing factor in A549 lung adenocarcinoma cells". Oncology Letters 16.1 (2018): 294-300.
Chicago
Hu, L., Tang, J., Huang, X., Zhang, T., Feng, X."Hypoxia exposure upregulates MALAT‑1 and regulates the transcriptional activity of PTB‑associated splicing factor in A549 lung adenocarcinoma cells". Oncology Letters 16, no. 1 (2018): 294-300. https://doi.org/10.3892/ol.2018.8637
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