Long non‑coding RNA H19 knockdown inhibits the cell viability and promotes apoptosis of thyroid cancer cells through regulating the PI3K/AKT pathway

  • Authors:
    • Xiaoyu Li
    • Qinghuai Li
    • Xiao Jin
    • Hao Guo
    • Yong Li
  • View Affiliations

  • Published online on: July 1, 2019     https://doi.org/10.3892/etm.2019.7720
  • Pages: 1863-1869
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Abstract

Certain long non‑coding (lnc)RNAs have been reported to serve important roles in the genesis and progression of thyroid cancer (TC). Recent studies have demonstrated that the expression of lncRNA H19 is upregulated in TC tissues; however, knowledge of the associated molecular mechanisms is limited. Therefore, the present study aimed to clarify the roles of H19 in TC. The mRNA expression of lncRNA H19 in TC tissues was determined using reverse transcription‑quantitative polymerase chain reaction analysis, and the effects of H19 knockdown on cell viability and apoptosis in vitro were assessed using MTT and flow cytometric assays, respectively. Finally, the signaling pathways involved in the effects of H19 were examined. The results indicated that H19 was upregulated in TC tissues. Silencing of H19 inhibited the cell viability and promoted apoptosis of FTC‑133 and TPC‑1 TC cells, accompanied by an increased expression of B‑cell lymphoma 2 (Bcl‑2)‑associated X protein and caspase 3, and repressed expression of Bcl‑2. The results of western blot analysis suggested that the levels of phosphorylated phosphoinositide‑3 kinase (PI3K) and phosphorylated AKT were attenuated by H19 silencing. These results suggest that lncRNA H19 exerts an oncogenic function in TC, in part through the PI3K/AKT pathway.
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September-2019
Volume 18 Issue 3

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Li X, Li Q, Jin X, Guo H and Li Y: Long non‑coding RNA H19 knockdown inhibits the cell viability and promotes apoptosis of thyroid cancer cells through regulating the PI3K/AKT pathway. Exp Ther Med 18: 1863-1869, 2019
APA
Li, X., Li, Q., Jin, X., Guo, H., & Li, Y. (2019). Long non‑coding RNA H19 knockdown inhibits the cell viability and promotes apoptosis of thyroid cancer cells through regulating the PI3K/AKT pathway. Experimental and Therapeutic Medicine, 18, 1863-1869. https://doi.org/10.3892/etm.2019.7720
MLA
Li, X., Li, Q., Jin, X., Guo, H., Li, Y."Long non‑coding RNA H19 knockdown inhibits the cell viability and promotes apoptosis of thyroid cancer cells through regulating the PI3K/AKT pathway". Experimental and Therapeutic Medicine 18.3 (2019): 1863-1869.
Chicago
Li, X., Li, Q., Jin, X., Guo, H., Li, Y."Long non‑coding RNA H19 knockdown inhibits the cell viability and promotes apoptosis of thyroid cancer cells through regulating the PI3K/AKT pathway". Experimental and Therapeutic Medicine 18, no. 3 (2019): 1863-1869. https://doi.org/10.3892/etm.2019.7720