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NICE‑3‑knockdown induces cell cycle arrest and autophagy in lung adenocarcinoma cells via the AKT/mTORC1 signaling pathway

  • Authors:
    • Longxia Du
    • Youru Wu
    • Xiaodan Han
    • Chen Wang
    • Aili Li
    • Guojin Huang
  • View Affiliations / Copyright

    Affiliations: Laboratory of Respiratory Diseases, The Affiliated Hospital of Guilin Medical University, Guilin, Guangxi 541001, P.R. China
    Copyright: © Du et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 625
    |
    Published online on: April 15, 2021
       https://doi.org/10.3892/etm.2021.10057
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Abstract

The NICE‑3 protein serves an oncogenic role in hepatocellular carcinoma, but its role in lung adenocarcinoma (LUAD) remains unknown. The aim of the present study was to investigate the potential role and underlying mechanisms of NICE‑3 in LUAD. In the present study, NICE‑3 expression in LUAD tissues and its association with patient prognosis were analyzed using datasets from The Cancer Genome Atlas and Gene Express Omnibus. After NICE‑3‑knockdown with small interfering RNA in LUAD cells, cell proliferation was measured by cell counting, cell cycle was examined by flow cytometry, cell invasion and migration were detected by Transwell assays and autophagic markers LC3 and p62, as well as phosphorylation of S6K and AKT, were determined by western blotting. The results of public database analysis demonstrated that compared with normal lung tissues, NICE‑3 expression was increased in LUAD tissues, where high expression levels were associated with a poor prognosis. The results of in vitro experimentation in LUAD cells indicated that NICE‑3‑knockdown inhibited proliferation, cell cycle, migration and invasion, but enhanced autophagy. Notably, NICE‑3‑knockdown inhibited AKT/mTORC1 signaling. The present results suggested that NICE‑3 may serve an oncogenic role in LUAD via the AKT/mTORC1 signaling pathway and may therefore be a potential therapeutic target for LUAD.
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Copy and paste a formatted citation
Spandidos Publications style
Du L, Wu Y, Han X, Wang C, Li A and Huang G: NICE‑3‑knockdown induces cell cycle arrest and autophagy in lung adenocarcinoma cells via the AKT/mTORC1 signaling pathway. Exp Ther Med 21: 625, 2021.
APA
Du, L., Wu, Y., Han, X., Wang, C., Li, A., & Huang, G. (2021). NICE‑3‑knockdown induces cell cycle arrest and autophagy in lung adenocarcinoma cells via the AKT/mTORC1 signaling pathway. Experimental and Therapeutic Medicine, 21, 625. https://doi.org/10.3892/etm.2021.10057
MLA
Du, L., Wu, Y., Han, X., Wang, C., Li, A., Huang, G."NICE‑3‑knockdown induces cell cycle arrest and autophagy in lung adenocarcinoma cells via the AKT/mTORC1 signaling pathway". Experimental and Therapeutic Medicine 21.6 (2021): 625.
Chicago
Du, L., Wu, Y., Han, X., Wang, C., Li, A., Huang, G."NICE‑3‑knockdown induces cell cycle arrest and autophagy in lung adenocarcinoma cells via the AKT/mTORC1 signaling pathway". Experimental and Therapeutic Medicine 21, no. 6 (2021): 625. https://doi.org/10.3892/etm.2021.10057
Copy and paste a formatted citation
x
Spandidos Publications style
Du L, Wu Y, Han X, Wang C, Li A and Huang G: NICE‑3‑knockdown induces cell cycle arrest and autophagy in lung adenocarcinoma cells via the AKT/mTORC1 signaling pathway. Exp Ther Med 21: 625, 2021.
APA
Du, L., Wu, Y., Han, X., Wang, C., Li, A., & Huang, G. (2021). NICE‑3‑knockdown induces cell cycle arrest and autophagy in lung adenocarcinoma cells via the AKT/mTORC1 signaling pathway. Experimental and Therapeutic Medicine, 21, 625. https://doi.org/10.3892/etm.2021.10057
MLA
Du, L., Wu, Y., Han, X., Wang, C., Li, A., Huang, G."NICE‑3‑knockdown induces cell cycle arrest and autophagy in lung adenocarcinoma cells via the AKT/mTORC1 signaling pathway". Experimental and Therapeutic Medicine 21.6 (2021): 625.
Chicago
Du, L., Wu, Y., Han, X., Wang, C., Li, A., Huang, G."NICE‑3‑knockdown induces cell cycle arrest and autophagy in lung adenocarcinoma cells via the AKT/mTORC1 signaling pathway". Experimental and Therapeutic Medicine 21, no. 6 (2021): 625. https://doi.org/10.3892/etm.2021.10057
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