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

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.