Long Noncoding RNA NR2F1-AS1 Enhances the Migration and Invasion of Hepatocellular Carcinoma via Modulating miR-642a/DEK Pathway

Author:

Xu Yingxia1,Han Chunrong2,Sun Jing3,Zhao Jingjing4,Liu Qing5,An Ping6ORCID

Affiliation:

1. Department of Infectious Diseases, Weifang People’s Hospital, Weifang 261041, China

2. Medical Records Room, Jinan Zhangqiu District Hospital of TCM, Jinan 250200, China

3. Department of Medical Administration, Qingdao Central Hospital, Qingdao University, Qingdao 266042, China

4. Department of Surgery, Zhangqiu District People’s Hospital, Jinan 250200, China

5. Department of Traditional Chinese Medicine, Zhangqiu District People’s Hospital, Jinan 250200, China

6. Department of Disinfection Supply Center, The 5th People’s Hospital of Ji’nan, Jinan 250022, China

Abstract

Purpose. Hepatocellular carcinoma (HCC), a malignant tumor that exists worldwide, has a high morbidity and mortality rate. Previous studies have reported that lncRNA NR2F1-AS1 plays a critical role in several cancers. Here, we aimed to investigate the biological function of NR2F1-AS1 and its molecular mechanism in the migration and invasion of HCC. Methods. Quantitative real-time PCR (qRT-PCR) was performed to analyze NR2F1-AS1 expression in HCC. The biological function was investigated by transwell invasion and migration assays. The protein level was identified by Western blot. In addition, the downstream targets of NR2F1-AS1 and miR-642a were confirmed by luciferase reporter assays. Results. NR2F1-AS1 was significantly upregulated in HCC and associated with the poor prognosis of HCC patients. Biological function experiments revealed that the silence of NR2F1-AS1 suppressed cell invasion and migration in HCC. More importantly, NR2F1-AS1 directly interacted with miR-642a and negatively regulated miR-642a. DEK was the target of miR-642a, and NR2F1-AS1 positively regulated DEK expression by suppressing miR-642a. Conclusion. Taken together, it is the first time we discovered the interaction of NR2F1-AS1 with miR-642a in modulating HCC cell invasion and migration.

Publisher

Hindawi Limited

Subject

Oncology

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