Silencing of long non‑coding RNA NEAT1 inhibits hepatocellular carcinoma progression by downregulating SMO by sponging microRNA‑503
- Chuihua Sun
- Ting Xiao
- Ying Xiao
- Yunbao Li
Affiliations: Department of Intensive Care Unit, Weifang People's Hospital, Weifang, Shandong 261041, P.R. China, Department of Infectious Diseases, Weifang People's Hospital, Weifang, Shandong 261041, P.R. China, Department of Ultrasound, 960 Hospital of The Chinese People's Liberation Army, Tai'an Hospital, Tai'an, Shandong 271000, P.R. China, Department of Clinical Laboratory, Jinan Chain Medical Laboratory Co., Ltd., Jinan, Shandong 250000, P.R. China
- Published online on: December 23, 2020 https://doi.org/10.3892/mmr.2020.11807
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Hepatocellular carcinoma (HCC) poses an increasing threat to humans, due to its poor prognosis. Nuclear‑enriched abundant transcript 1 (NEAT1), a type of long non‑coding (lnc)RNA, has been found to function in a variety of cancer types. However, the role of NEAT1 in HCC is poorly understood. Reverse transcription‑quantitative PCR was used to detect the expression levels of NEAT1, microRNA (miR)‑503 and Smoothened (SMO) mRNA in HCC tissues and cells. MTT and flow cytometry assays were used to investigate cell viability and apoptosis, respectively, while Transwell assays were performed to investigate cell invasion and migration. StarBase and TargetScan were utilized to predict the target sequence between miR‑503 and NEAT1 or SMO, the results of which were verified using a dual‑luciferase reporter assay. The protein expression level of SMO was measured using western blot. The RNA expression level of NEAT1 and SMO was significantly elevated in HCC tissues and cells compared with that in the corresponding healthy tissues and cells, which was contrary to miR‑503 expression level. NEAT1 silencing was found to restrict the viability, migration and invasion of the cells, while simultaneously induced apoptosis in the HCC cell line. Further studies found that miR‑503 expression was negatively correlated with NEAT1 or SMO. It was also confirmed that NEAT1 directly interacted with miR‑503 and miR‑503 could bind to the 3'‑untranslated region of SMO. Furthermore, overexpression of NEAT1 or SMO could reverse the effects of miR‑503‑mediated inhibition on cell viability, invasion, migration and promotion of apoptosis in the HCC cell lines. These results demonstrated that downregulation of NEAT1 impeded the viability, migration, invasion and induced apoptosis through the NEAT1/miR‑503/SMO axis in the HCC cell line.