Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

LncRNA NBAT-1 inhibits the progression of hepatocellular carcinoma by interacting with CYLD

Jisan Sun^1,2, Guoyao Li², Li Zhang², Yan Xie², Chiyi Chen², Jian He², Wentao Jiang²

¹Tianjin Medical University First Center Clinical Hospital; ²Department of Liver Transplantation, Tianjin First Center Hospital, Tianjin, China.

For correspondence:- Wentao Jiang Email: Jiangwentao@vip.163.com Tel:+862223626857

Accepted: 29 July 2021 Published: 31 August 2021

Citation: Sun J, Li G, Zhang L, Xie Y, Chen C, He J, et al. LncRNA NBAT-1 inhibits the progression of hepatocellular carcinoma by interacting with CYLD. Trop J Pharm Res 2021; 20(8):1585-1591 doi: 10.4314/tjpr.v20i8.6

© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To illustrate the biological influences of long non-coding RNA (lncRNA) NBAT-1 (neuroblastoma associated transcript 1) on HCC progression and the molecular mechanism of action.

Methods: NBAT-1 levels in HCC tissues and cell lines were determined by quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between NBAT-1 and prognosis in HCC was analyzed. After knockdown of NBAT-1 in HepG2 and Hep3B cells, proliferative and migratory changes were assessed by cell counting kit-8 (CCK-8) and Transwell assay, respectively. The interaction between NBAT-1 and CYLD was confirmed by subcellular fraction determination and RNA binding protein immunoprecipitation (RIP). Rescue experiments were conducted to verify the involvement of CYLD in HCC cell functions regulated by NBAT-1.

Results: NBAT-1 was downregulated in HCC tissues. Its level was much lower in metastatic or advanced stage HCC patients (p < 0.05), showing a certain prognostic potential. Knockdown of NBAT-1 stimulated proliferative and migratory potentials in HepG2 and Hep3B cells. NBAT-1 was mainly distributed in the cell cytoplasm. The mRNA and protein levels of CYLD were downregulated in HCC cells by NBAT-1 knockdown, displaying a positive interaction. CYLD was involved in the regulatory effect of NBAT-1 on HCC progression.

Conclusion: Through a positive interaction with CYLD, NBAT-1 inhibits the malignant progression of HCC. These findings provide a potential approach to the development of targeted therapies for HCC.

Keywords: Hepatocellular carcinoma, NBAT-1, CYLD, Cell proliferation, Cell migration