Chunhui Zhou1, Zhen Chen2, Changli Peng1, Changyong Chen1, Haiping Li1. 1. Department of Radiology, Xiangya Hospital, Central South University, Changsha, China. 2. Department of Clinical Laboratory, Xiangya Hospital, Central South University, Changsha, China.
Abstract
Background: 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. Aim of the Study: The aim of the study is to explore the role and molecular regulatory mechanism of TRIM52-AS1 in HCC. Materials and Methods: Real-time quantitative polymerase chain reaction examined TRIM52-AS1, miR-514a-5p, and mitochondrial ribosomal protein S18a (MRPS18A) 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 TRIM52-AS1 in HCC. RNA immunoprecipitation (RIP), RNA pull down, and luciferase reporter assays validated the association among TRIM52-AS1, miR-514a-5p, and MRPS18A. Nuclear-cytoplasmic fractionation assay revealed the subcellular location of TRIM52-AS1 in HCC cells. Results: TRIM52-AS1 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 TRIM52-AS1 ablation depressed cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition process in vitro and inhibited tumor growth in vivo. Furthermore, the authors validated TRIM52-AS1 bound with miR-514a-5p in HCC. TRIM52-AS1 inversely regulated miR-514a-5p expression. Afterward, MRPS18A was identified to be a downstream target of miR-514a-5p. Ultimately, rescue assays manifested that MRPS18A upregulation could neutralize the attenuated effects resulting from TRIM52-AS1 deficiency. Conclusions: All in all, TRIM52-AS1 sponged miR-514a-5p to facilitate HCC progression through increasing MRPS18A expression. The findings highlight TRIM52-AS1 as a novel therapeutic target for HCC.
Background: 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. Aim of the Study: The aim of the study is to explore the role and molecular regulatory mechanism of TRIM52-AS1 in HCC. Materials and Methods: Real-time quantitative polymerase chain reaction examined TRIM52-AS1, miR-514a-5p, and mitochondrial ribosomal protein S18a (MRPS18A) 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 TRIM52-AS1 in HCC. RNA immunoprecipitation (RIP), RNA pull down, and luciferase reporter assays validated the association among TRIM52-AS1, miR-514a-5p, and MRPS18A. Nuclear-cytoplasmic fractionation assay revealed the subcellular location of TRIM52-AS1 in HCC cells. Results:TRIM52-AS1 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 TRIM52-AS1 ablation depressed cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition process in vitro and inhibited tumor growth in vivo. Furthermore, the authors validated TRIM52-AS1 bound with miR-514a-5p in HCC. TRIM52-AS1 inversely regulated miR-514a-5p expression. Afterward, MRPS18A was identified to be a downstream target of miR-514a-5p. Ultimately, rescue assays manifested that MRPS18A upregulation could neutralize the attenuated effects resulting from TRIM52-AS1 deficiency. Conclusions: All in all, TRIM52-AS1 sponged miR-514a-5p to facilitate HCC progression through increasing MRPS18A expression. The findings highlight TRIM52-AS1 as a novel therapeutic target for HCC.