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

Du,Longxia; Wu,Youru; Han,Xiaodan; Wang,Chen; Li,Aili; Huang,Guojin

doi:10.3892/etm.2021.10057

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

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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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