Abstract

Background: Therapy for patients with liver cancer in the advanced stage remains a great challenge, and there are very few approved treatments. Although accumulated evidence demonstrates the importance of lncRNAs in liver cancer, data on the functional roles and molecular mechanisms of endogenous bornavirus-like nucleoprotein () have been rarely reported.

Materials And Methods: The bioinformatics prediction software ENCORI was used to predict the putative binding sites of . The regulatory roles of EBLN3P and in cell proliferation, migration and invasion ability were verified by the Cell Counting Kit-8, wound healing and Transwell assays, respectively. The interactions among , and were explored by a luciferase assay and Western blotting. The expression of and microRNA (miR)-144-3p in liver cancer tissues was quantified by reverse transcription-quantitative PCR, and the expression of dedicator of cytokinesis 4 (DOCK4) was quantified by immunohistochemical analysis.

Results: The present results revealed that overexpression of or knockdown of promoted liver cancer cell proliferation, migration and invasion. Bioinformatics analysis and a luciferase assay demonstrated that directly interacts with to attenuate binding to the 3'-untranslated region of . Furthermore, the mechanistic investigations showing that the miR-144-3p/DOCK4 regulatory loop was activated by knockdown of miR-144-3p or overexpression of validate the roles of in promoting liver cancer cell proliferation, migration and invasion in vitro. Elevated levels of and and decreased expression were observed in both liver cancer tissues and cell lines.

Conclusion: The present study is the first to demonstrate that may act as a ceRNA to modulate expression by competitively sponging , leading to the regulation of liver cancer progression, which provides new insights for liver cancer diagnosis and treatment.