Open Access

Knockdown of long non‑coding RNA NEAT1 relieves inflammation of ulcerative colitis by regulating the miR‑603/FGF9 pathway

  • Authors:
    • Fengdong Li
    • Hui Liu
    • Jinjin Fu
    • Li Fan
    • Shuangshuang Lu
    • Huahui Zhang
    • Zhanju Liu
  • View Affiliations

  • Published online on: December 10, 2021     https://doi.org/10.3892/etm.2021.11054
  • Article Number: 131
  • Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Ulcerative colitis (UC) is a significant threat to human life. Hence, there is an urgent requirement to understand the mechanism of UC progression and to develop novel therapeutic interventions for the treatment of UC. The present study aimed to evaluate the potential significance of long non‑coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) in the progression of UC. NEAT1 expression was detected in colonic mucosa samples from patients with UC and healthy individuals. Fetal human cells (FHCs) were treated with different concentrations of lipopolysaccharides (LPS) to induce UC‑caused inflammatory injury, and the effects of NEAT1 knockdown were investigated on cytokines production, cell apoptosis and viability. Furthermore, the correlation and regulation between NEAT1 and microRNA (miRNA/miR)‑603 and the fibroblast growth factor 9 (FGF9) pathway were investigated. The results demonstrated that NEAT1 expression was upregulated in the colonic mucosa tissues of patients with UC. In addition, significant cell injury was observed in FHCs treated with different concentrations of LPS, with decreased cell viability, and increased apoptosis and inflammatory cytokines production. Conversely, NEAT1 knockdown significantly reduced LPS‑induced cell injury in FHCs, which was achieved through negative regulation of miR‑603 expression. Furthermore, FGF9 was negatively regulated by miR‑603, and thus, FGF9 was identified as a potential target of miR‑603. Notably, FGF9 knockdown reversed the suppressing effects of miR‑603 on LPS‑induced injury in FHCs. Taken together, the results of the present study suggest that NEAT1 contributes to the development of UC by regulating the miR‑603/FGF9 pathway.
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February-2022
Volume 23 Issue 2

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

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Spandidos Publications style
Li F, Liu H, Fu J, Fan L, Lu S, Zhang H and Liu Z: Knockdown of long non‑coding RNA NEAT1 relieves inflammation of ulcerative colitis by regulating the miR‑603/FGF9 pathway. Exp Ther Med 23: 131, 2022
APA
Li, F., Liu, H., Fu, J., Fan, L., Lu, S., Zhang, H., & Liu, Z. (2022). Knockdown of long non‑coding RNA NEAT1 relieves inflammation of ulcerative colitis by regulating the miR‑603/FGF9 pathway. Experimental and Therapeutic Medicine, 23, 131. https://doi.org/10.3892/etm.2021.11054
MLA
Li, F., Liu, H., Fu, J., Fan, L., Lu, S., Zhang, H., Liu, Z."Knockdown of long non‑coding RNA NEAT1 relieves inflammation of ulcerative colitis by regulating the miR‑603/FGF9 pathway". Experimental and Therapeutic Medicine 23.2 (2022): 131.
Chicago
Li, F., Liu, H., Fu, J., Fan, L., Lu, S., Zhang, H., Liu, Z."Knockdown of long non‑coding RNA NEAT1 relieves inflammation of ulcerative colitis by regulating the miR‑603/FGF9 pathway". Experimental and Therapeutic Medicine 23, no. 2 (2022): 131. https://doi.org/10.3892/etm.2021.11054