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LncRNA SNHG6 inhibits cell proliferation and metastasis by targeting ETS1 via the PI3K/AKT/mTOR pathway in colorectal cancer

  • Authors:
    • Su Meng
    • Zhao Jian
    • Xiaofei Yan
    • Jibin Li
    • Rui Zhang
  • View Affiliations / Copyright

    Affiliations: Department of Medical Oncology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, P.R. China
    Copyright: © Meng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2541-2548
    |
    Published online on: July 19, 2019
       https://doi.org/10.3892/mmr.2019.10510
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Abstract

The term ‘long non‑coding RNAs’ (lncRNAs) refers to all non‑protein coding transcripts >200 nucleotides in length. Dysregulation of lncRNAs has been identified in colorectal cancer, which is one of the more serious types of cancer worldwide, third place in the mortality rates, and is associated with poor prognoses. Novel evidence suggests that lncRNAs serve an important role in regulating the development and progression of colorectal cancer. In the present study, it was demonstrated that SNHG6 expression was downregulated in colorectal cancer tissues by reverse transcription quantitative polymerase chain reaction assays; however, ETS1 expression levels were upregulated. Overexpression of SNHG6 not only inhibited the proliferation of colon cancer cells in vitro by inducing apoptosis, but also inhibited cell proliferation, invasion and migration. The overexpression of SNHG6 inhibited colon cell viability and proliferation by targeting ETS1 through the phosphoinositide 3‑kinase/protein kinase B/mechanistic target of rapamycin signaling pathway. These results suggested that SNHG6 may directly suppress ETS1, which may be one of potential mechanisms through which it inhibits the viability and proliferation of colorectal cancer cells, and it provides novel insight into the carcinogenesis of colorectal cancer. In addition, it may assist in the development of a treatment approach for ETS1‑activated colorectal cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Meng S, Jian Z, Yan X, Li J and Zhang R: LncRNA SNHG6 inhibits cell proliferation and metastasis by targeting ETS1 via the PI3K/AKT/mTOR pathway in colorectal cancer. Mol Med Rep 20: 2541-2548, 2019.
APA
Meng, S., Jian, Z., Yan, X., Li, J., & Zhang, R. (2019). LncRNA SNHG6 inhibits cell proliferation and metastasis by targeting ETS1 via the PI3K/AKT/mTOR pathway in colorectal cancer. Molecular Medicine Reports, 20, 2541-2548. https://doi.org/10.3892/mmr.2019.10510
MLA
Meng, S., Jian, Z., Yan, X., Li, J., Zhang, R."LncRNA SNHG6 inhibits cell proliferation and metastasis by targeting ETS1 via the PI3K/AKT/mTOR pathway in colorectal cancer". Molecular Medicine Reports 20.3 (2019): 2541-2548.
Chicago
Meng, S., Jian, Z., Yan, X., Li, J., Zhang, R."LncRNA SNHG6 inhibits cell proliferation and metastasis by targeting ETS1 via the PI3K/AKT/mTOR pathway in colorectal cancer". Molecular Medicine Reports 20, no. 3 (2019): 2541-2548. https://doi.org/10.3892/mmr.2019.10510
Copy and paste a formatted citation
x
Spandidos Publications style
Meng S, Jian Z, Yan X, Li J and Zhang R: LncRNA SNHG6 inhibits cell proliferation and metastasis by targeting ETS1 via the PI3K/AKT/mTOR pathway in colorectal cancer. Mol Med Rep 20: 2541-2548, 2019.
APA
Meng, S., Jian, Z., Yan, X., Li, J., & Zhang, R. (2019). LncRNA SNHG6 inhibits cell proliferation and metastasis by targeting ETS1 via the PI3K/AKT/mTOR pathway in colorectal cancer. Molecular Medicine Reports, 20, 2541-2548. https://doi.org/10.3892/mmr.2019.10510
MLA
Meng, S., Jian, Z., Yan, X., Li, J., Zhang, R."LncRNA SNHG6 inhibits cell proliferation and metastasis by targeting ETS1 via the PI3K/AKT/mTOR pathway in colorectal cancer". Molecular Medicine Reports 20.3 (2019): 2541-2548.
Chicago
Meng, S., Jian, Z., Yan, X., Li, J., Zhang, R."LncRNA SNHG6 inhibits cell proliferation and metastasis by targeting ETS1 via the PI3K/AKT/mTOR pathway in colorectal cancer". Molecular Medicine Reports 20, no. 3 (2019): 2541-2548. https://doi.org/10.3892/mmr.2019.10510
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