Long Noncoding RNA TRIM52-AS1 Sponges miR-514a-5p to Facilitate Hepatocellular Carcinoma Progression Through Increasing MRPS18A

Abstract

<b><i>Background:</i></b> Hepatocellular carcinoma (HCC) is associated with high morbidity and mortality and has become the most frequently diagnosed liver cancer globally. Long noncoding RNAs have been widely studied because they exert essential functions in human diseases. <b><i>Aim of the Study:</i></b> The aim of the study is to explore the role and molecular regulatory mechanism of <i>TRIM52-AS1</i> in HCC. <b><i>Materials and Methods:</i></b> Real-time quantitative polymerase chain reaction examined <i>TRIM52-AS1</i>, <i>miR-514a-5p</i>, and mitochondrial ribosomal protein S18a (<i>MRPS18A</i>) expression in HCC cells. Cell Counting Kit-8 (CCK-8), colony formation, flow cytometry, JC-1, transwell, and Western blot assays uncovered the function of <i>TRIM52-AS1</i> in HCC. RNA immunoprecipitation (RIP), RNA pull down, and luciferase reporter assays validated the association among <i>TRIM52-AS1</i>, <i>miR-514a-5p</i>, and <i>MRPS18A</i>. Nuclear-cytoplasmic fractionation assay revealed the subcellular location of <i>TRIM52-AS1</i> in HCC cells. <b><i>Results:</i></b> <i>TRIM52-AS1</i> was revealed to be upregulated in HCC tissue samples according to GEPIA database. Consistent results were recognized in HCC cell lines. Subsequently, loss-of-function assays confirmed that <i>TRIM52-AS1</i> ablation depressed cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition process <i>in vitro</i> and inhibited tumor growth <i>in vivo</i>. Furthermore, the authors validated <i>TRIM52-AS1</i> bound with <i>miR-514a-5p</i> in HCC. <i>TRIM52-AS1</i> inversely regulated <i>miR-514a-5p</i> expression. Afterward, <i>MRPS18A</i> was identified to be a downstream target of <i>miR-514a-5p</i>. Ultimately, rescue assays manifested that <i>MRPS18A</i> upregulation could neutralize the attenuated effects resulting from <i>TRIM52-AS1</i> deficiency. <b><i>Conclusions:</i></b> All in all, <i>TRIM52-AS1</i> sponged <i>miR-514a-5p</i> to facilitate HCC progression through increasing <i>MRPS18A</i> expression. The findings highlight <i>TRIM52-AS1</i> as a novel therapeutic target for HCC.