{"title":"Role and Clinical Significance of miR-144-3p in Primary Hepatocellular Carcinoma","authors":"Xianghua Sun, Fushun Li, Qing Liu, Xilu Liu, G. Dong, Yu Zhang","doi":"10.1166/NNL.2020.3256","DOIUrl":null,"url":null,"abstract":"The morbidity of liver cancer (LC) is increasing and its high mortality poses a significant health threat worldwide. Therefore, it is crucial to identify the underlying mechanism of LC development and progression. The expression of miR-144-3p and ZEB1 gene in LC and paracanerous tissues\n was measured by Polymerase chain reaction (PCR). We transfected miR-144-3p-mimics, miR-NC, si-ZEB1, and si-NC into HepG2, Huh-7, and HL-7702 normal liver cells to establish a cell model. Protein expression was examined by western blot (WB) analysis. Cell proliferation, invasion, and apoptosis\n were assessed by CCK-8, Transwell, and flow cytometry assays. The relationship between miR-144-3p and ZEB1 was determined using a dual-luciferase reporter assay. We found that miR-144-3p expression decreased dramatically, whereas ZEB1 increased in hepatocellular carcinoma (HCC). Moreover,\n over-expressing miR-144-3p suppressed cell growth and induced apoptosis. The expression of apoptosis-related proteins was consistent with the induction of apoptosis. The relationship between miR-144-3p and ZEB1 was confirmed using a dual-luciferase reporter assay. Finally, rescue experiments\n revealed that over-expressing ZEB1 counteracted miR-144-3p inhibition on LC cell growth, invasion, and apoptosis induction. We conclude that miR-144-3p suppresses HCC cell growth and invasion and promotes apoptosis by regulating ZEB1 expression, suggesting that this interaction may represent\n a target for HCC treatment.","PeriodicalId":18871,"journal":{"name":"Nanoscience and Nanotechnology Letters","volume":"12 1","pages":"1413-1421"},"PeriodicalIF":0.0000,"publicationDate":"2020-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nanoscience and Nanotechnology Letters","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1166/NNL.2020.3256","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
The morbidity of liver cancer (LC) is increasing and its high mortality poses a significant health threat worldwide. Therefore, it is crucial to identify the underlying mechanism of LC development and progression. The expression of miR-144-3p and ZEB1 gene in LC and paracanerous tissues
was measured by Polymerase chain reaction (PCR). We transfected miR-144-3p-mimics, miR-NC, si-ZEB1, and si-NC into HepG2, Huh-7, and HL-7702 normal liver cells to establish a cell model. Protein expression was examined by western blot (WB) analysis. Cell proliferation, invasion, and apoptosis
were assessed by CCK-8, Transwell, and flow cytometry assays. The relationship between miR-144-3p and ZEB1 was determined using a dual-luciferase reporter assay. We found that miR-144-3p expression decreased dramatically, whereas ZEB1 increased in hepatocellular carcinoma (HCC). Moreover,
over-expressing miR-144-3p suppressed cell growth and induced apoptosis. The expression of apoptosis-related proteins was consistent with the induction of apoptosis. The relationship between miR-144-3p and ZEB1 was confirmed using a dual-luciferase reporter assay. Finally, rescue experiments
revealed that over-expressing ZEB1 counteracted miR-144-3p inhibition on LC cell growth, invasion, and apoptosis induction. We conclude that miR-144-3p suppresses HCC cell growth and invasion and promotes apoptosis by regulating ZEB1 expression, suggesting that this interaction may represent
a target for HCC treatment.