lncRNA NEAT1 regulates the proliferation and migration of hepatocellular carcinoma cells by acting as a miR‑320a molecular sponge and targeting L antigen family member 3

Long non-coding RNAs (IncRNAs) serve a pivotal role in hepatocellular carcinoma (HCC) progression and have been confirmed to participate in the carcinogenesis and development of HCC. Certain studies have focused on lncRNA nuclear enriched abundant transcript 1 (NEAT1) in HCC. However, the relationsh...

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Veröffentlicht in:International journal of oncology 2020-10, Vol.57 (4), p.1001-1012
Hauptverfasser: Zhang, Yixi, Huang, Changjun, Zhu, Zebin, Hou, Yufei, Huang, Shanzhou, Sun, Chengjun, Tang, Yunhua, Zhang, Zhiheng, Wang, Linhe, Chen, Huadi, Ju, Weiqiang, Qiao, Xin, Chen, Maogen
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container_end_page 1012
container_issue 4
container_start_page 1001
container_title International journal of oncology
container_volume 57
creator Zhang, Yixi
Huang, Changjun
Zhu, Zebin
Hou, Yufei
Huang, Shanzhou
Sun, Chengjun
Tang, Yunhua
Zhang, Zhiheng
Wang, Linhe
Chen, Huadi
Ju, Weiqiang
Qiao, Xin
Chen, Maogen
description Long non-coding RNAs (IncRNAs) serve a pivotal role in hepatocellular carcinoma (HCC) progression and have been confirmed to participate in the carcinogenesis and development of HCC. Certain studies have focused on lncRNA nuclear enriched abundant transcript 1 (NEAT1) in HCC. However, the relationship between lncRNA NEAT1 and HCC remains unclear. The present study found that NEAT1 was significantly overexpressed in HCC cell lines compared with LX-2 hepatic stellate cells. NEAT1 expression in Huh7 and MHCC-97H cells was increased following transfection with lentivirus (LV)-NEAT1 but inhibited by LV-short hairpin NEAT1. Knockdown of NEAT1 significantly repressed HCC cell viability, increased cell apoptosis, and inhibited cell migration and invasion capacity. By contrast, upregulation of NEAT1 demonstrated the reverse effects. Furthermore, microRNA-320a (miR-230a) was predicted to be a direct target of NEAT1 and was significantly reduced in HCC cells. Additionally, a luciferase activity reporter assay and RNA immunoprecipitation assay were performed to confirm the interaction between miR-320a and NEAT1. Using a dual-luciferase activity assay, L antigen family member 3 (LAGE3) was found to be a target of miR-320a. Finally, in vivo nude mouse models were established, and the results indicated that NEAT1 suppressed HCC progression by targeting miR-320a. In conclusion, the present findings revealed that the NEAT1/miR-320a/LAGE3 axis participates in HCC development and that NEAT1 could be used as a biomarker for HCC. Key words: long non-coding RNA nuclear enriched abundant transcript 1, L antigen family member 3, micorRNA-320a, proliferation, migration, hepatocellular carcinoma
doi_str_mv 10.3892/ijo.2020.5108
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Certain studies have focused on lncRNA nuclear enriched abundant transcript 1 (NEAT1) in HCC. However, the relationship between lncRNA NEAT1 and HCC remains unclear. The present study found that NEAT1 was significantly overexpressed in HCC cell lines compared with LX-2 hepatic stellate cells. NEAT1 expression in Huh7 and MHCC-97H cells was increased following transfection with lentivirus (LV)-NEAT1 but inhibited by LV-short hairpin NEAT1. Knockdown of NEAT1 significantly repressed HCC cell viability, increased cell apoptosis, and inhibited cell migration and invasion capacity. By contrast, upregulation of NEAT1 demonstrated the reverse effects. Furthermore, microRNA-320a (miR-230a) was predicted to be a direct target of NEAT1 and was significantly reduced in HCC cells. Additionally, a luciferase activity reporter assay and RNA immunoprecipitation assay were performed to confirm the interaction between miR-320a and NEAT1. Using a dual-luciferase activity assay, L antigen family member 3 (LAGE3) was found to be a target of miR-320a. Finally, in vivo nude mouse models were established, and the results indicated that NEAT1 suppressed HCC progression by targeting miR-320a. In conclusion, the present findings revealed that the NEAT1/miR-320a/LAGE3 axis participates in HCC development and that NEAT1 could be used as a biomarker for HCC. 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Certain studies have focused on lncRNA nuclear enriched abundant transcript 1 (NEAT1) in HCC. However, the relationship between lncRNA NEAT1 and HCC remains unclear. The present study found that NEAT1 was significantly overexpressed in HCC cell lines compared with LX-2 hepatic stellate cells. NEAT1 expression in Huh7 and MHCC-97H cells was increased following transfection with lentivirus (LV)-NEAT1 but inhibited by LV-short hairpin NEAT1. Knockdown of NEAT1 significantly repressed HCC cell viability, increased cell apoptosis, and inhibited cell migration and invasion capacity. By contrast, upregulation of NEAT1 demonstrated the reverse effects. Furthermore, microRNA-320a (miR-230a) was predicted to be a direct target of NEAT1 and was significantly reduced in HCC cells. Additionally, a luciferase activity reporter assay and RNA immunoprecipitation assay were performed to confirm the interaction between miR-320a and NEAT1. Using a dual-luciferase activity assay, L antigen family member 3 (LAGE3) was found to be a target of miR-320a. Finally, in vivo nude mouse models were established, and the results indicated that NEAT1 suppressed HCC progression by targeting miR-320a. In conclusion, the present findings revealed that the NEAT1/miR-320a/LAGE3 axis participates in HCC development and that NEAT1 could be used as a biomarker for HCC. 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Certain studies have focused on lncRNA nuclear enriched abundant transcript 1 (NEAT1) in HCC. However, the relationship between lncRNA NEAT1 and HCC remains unclear. The present study found that NEAT1 was significantly overexpressed in HCC cell lines compared with LX-2 hepatic stellate cells. NEAT1 expression in Huh7 and MHCC-97H cells was increased following transfection with lentivirus (LV)-NEAT1 but inhibited by LV-short hairpin NEAT1. Knockdown of NEAT1 significantly repressed HCC cell viability, increased cell apoptosis, and inhibited cell migration and invasion capacity. By contrast, upregulation of NEAT1 demonstrated the reverse effects. Furthermore, microRNA-320a (miR-230a) was predicted to be a direct target of NEAT1 and was significantly reduced in HCC cells. Additionally, a luciferase activity reporter assay and RNA immunoprecipitation assay were performed to confirm the interaction between miR-320a and NEAT1. Using a dual-luciferase activity assay, L antigen family member 3 (LAGE3) was found to be a target of miR-320a. Finally, in vivo nude mouse models were established, and the results indicated that NEAT1 suppressed HCC progression by targeting miR-320a. In conclusion, the present findings revealed that the NEAT1/miR-320a/LAGE3 axis participates in HCC development and that NEAT1 could be used as a biomarker for HCC. Key words: long non-coding RNA nuclear enriched abundant transcript 1, L antigen family member 3, micorRNA-320a, proliferation, migration, hepatocellular carcinoma</abstract><cop>Athens</cop><pub>Spandidos Publications</pub><doi>10.3892/ijo.2020.5108</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record>
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source Spandidos Publications Journals; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection
subjects Antigens
Apoptosis
Biotechnology industries
Cell culture
Cell growth
Cloning
Colorectal cancer
Comparative analysis
Development and progression
Gene expression
Hepatocellular carcinoma
Kinases
Liver cancer
MicroRNA
MicroRNAs
Plasmids
Scientific equipment industry
Software industry
Tumorigenesis
title lncRNA NEAT1 regulates the proliferation and migration of hepatocellular carcinoma cells by acting as a miR‑320a molecular sponge and targeting L antigen family member 3
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