Downregulation of long non‑coding RNA GACAT1 suppresses proliferation and induces apoptosis of NSCLC cells by sponging microRNA‑422a
- Youqing Zhong
- Hui Lin
- Qi Li
- Chang Liu
- Lei Zhong
Affiliations: Department of Respiratory Medicine, The First Affiliated Hospital of Hainan Medical University, Haikou, Hainan 571100, P.R. China, Department of Anesthesia, Hainan General Hospital, Haikou, Hainan 570311, P.R. China, Clinical Laboratory, Ganzhou People's Hospital of Jiangxi Province, Ganzhou, Jiangxi 341000, P.R. China
- Published online on: December 22, 2020 https://doi.org/10.3892/ijmm.2020.4826
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Increasing evidence has demonstrated the important roles of long non‑coding (lnc) RNA in non‑small cell lung cancer (NSCLC). lncRNA gastric cancer‑associated transcript 1 (GACAT1) has been reported to play an oncogenic role in different types of cancer; however, the function of GACAT1 in NSCLC remains unclear. The present study found that GACAT1 was overexpressed in NSCLC tissues and was associated with poor outcomes in patients with NSCLC. Functional experiments revealed that GACAT1 downregulation inhibited proliferation, induced apoptosis and cell cycle arrest of 2 NSCLC cell lines. GACAT1 was found to target microRNA(miR)‑422a mechanically and negatively regulated miR‑422a expression. Reduced expression of miR‑422a in NSCLC tissues was inversely correlated with that of GACAT1. Furthermore, YY1 transcription factor (YY1) was identified as a downstream miR‑422a target. Reduced expression of GACAT1 inactivated YY1 by sponging miR‑422a in NSCLC cells. YY1 reintroduction reversed the reduced proliferation of NSCLC cells via GACAT1 knockdown. Taken together, these results revealed the novel role of the GACAT1/miR‑422a pathway in the progression of NSCLC cell lines, providing a possible therapeutic strategy for NSCLC treatment.