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Article

Long non‑coding RNA DLX6‑AS1 silencing inhibits malignant phenotypes of gastric cancer cells

  • Authors:
    • Xiaodan Fu
    • Yifu Tian
    • Weilu Kuang
    • Sailan Wen
    • Wei Guo
  • View Affiliations / Copyright

    Affiliations: Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan 410005, P.R. China, Department of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410005, P.R. China, Department of Pathology, Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China, Department of Pathology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, Hunan 410002, P.R. China
  • Pages: 4715-4722
    |
    Published online on: April 23, 2019
       https://doi.org/10.3892/etm.2019.7521
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Abstract

It has been revealed that long non‑coding RNAs (lncRNAs) serve a key role in various malignancies, including gastric cancer (GC). In the present study, the expression and function of lncRNA distal‑less homeobox 6 antisense 1 (DLX6‑AS1) in GC was investigated. The data revealed that the expression of DLX6‑AS1 was significantly upregulated in GC tissues compared with adjacent paired noncancerous tissues. Furthermore, the expression of DLX6‑AS1 was higher in advanced GC tissue samples (III/IV) compared with the expression in early‑stage samples (I/II). Furthermore, the current study demonstrated that a high expression of DLX6‑AS1 was significantly associated with advanced clinical stage, lymph node metastasis and distant metastasis. Compared with patients with a low DLX6‑AS1 expression, DLX6‑AS1 expression in patients with GC was associated with decreased survival. In vitro experimental data indicated that DLX6‑AS1 was upregulated in GC cell lines and that the inhibition of DLX6‑AS1 markedly reduced GC cell proliferation, colony formation, cell cycle progression, migration and invasion. Further investigation revealed that knockdown of DLX6‑AS1 inhibited EMT in GC cells. In summary, the present study demonstrated that lncRNA DLX6‑AS1 was upregulated and serves an oncogenic role in GC, indicating that DLX6‑AS1 may be a novel therapeutic target for GC treatment.
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Copy and paste a formatted citation
Spandidos Publications style
Fu X, Tian Y, Kuang W, Wen S and Guo W: Long non‑coding RNA DLX6‑AS1 silencing inhibits malignant phenotypes of gastric cancer cells. Exp Ther Med 17: 4715-4722, 2019.
APA
Fu, X., Tian, Y., Kuang, W., Wen, S., & Guo, W. (2019). Long non‑coding RNA DLX6‑AS1 silencing inhibits malignant phenotypes of gastric cancer cells. Experimental and Therapeutic Medicine, 17, 4715-4722. https://doi.org/10.3892/etm.2019.7521
MLA
Fu, X., Tian, Y., Kuang, W., Wen, S., Guo, W."Long non‑coding RNA DLX6‑AS1 silencing inhibits malignant phenotypes of gastric cancer cells". Experimental and Therapeutic Medicine 17.6 (2019): 4715-4722.
Chicago
Fu, X., Tian, Y., Kuang, W., Wen, S., Guo, W."Long non‑coding RNA DLX6‑AS1 silencing inhibits malignant phenotypes of gastric cancer cells". Experimental and Therapeutic Medicine 17, no. 6 (2019): 4715-4722. https://doi.org/10.3892/etm.2019.7521
Copy and paste a formatted citation
x
Spandidos Publications style
Fu X, Tian Y, Kuang W, Wen S and Guo W: Long non‑coding RNA DLX6‑AS1 silencing inhibits malignant phenotypes of gastric cancer cells. Exp Ther Med 17: 4715-4722, 2019.
APA
Fu, X., Tian, Y., Kuang, W., Wen, S., & Guo, W. (2019). Long non‑coding RNA DLX6‑AS1 silencing inhibits malignant phenotypes of gastric cancer cells. Experimental and Therapeutic Medicine, 17, 4715-4722. https://doi.org/10.3892/etm.2019.7521
MLA
Fu, X., Tian, Y., Kuang, W., Wen, S., Guo, W."Long non‑coding RNA DLX6‑AS1 silencing inhibits malignant phenotypes of gastric cancer cells". Experimental and Therapeutic Medicine 17.6 (2019): 4715-4722.
Chicago
Fu, X., Tian, Y., Kuang, W., Wen, S., Guo, W."Long non‑coding RNA DLX6‑AS1 silencing inhibits malignant phenotypes of gastric cancer cells". Experimental and Therapeutic Medicine 17, no. 6 (2019): 4715-4722. https://doi.org/10.3892/etm.2019.7521
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