LncRNA FGD5-AS1 functions as an oncogene to upregulate GTPBP4 expression by sponging miR-873-5p in hepatocellular carcinoma
The long non-coding FGD5-AS1 (LncFGD5-AS1) has been reported to be a novel carcinogenic gene and participant in regulating tumor progression by sponging microRNAs (miRNAs). However, the pattern of expression and the biological role of FGD5-AS1 in hepatocellular carcinoma (HCC) remains largely unkno...
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2021
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oai:doaj.org-article:aba31fe3b7a944a5b44f019aa68d98ec2021-11-17T07:41:24ZLncRNA FGD5-AS1 functions as an oncogene to upregulate GTPBP4 expression by sponging miR-873-5p in hepatocellular carcinoma 10.4081/ejh.2021.33001121-760X2038-8306https://doaj.org/article/aba31fe3b7a944a5b44f019aa68d98ec2021-11-01T00:00:00Zhttps://ejh.it/index.php/ejh/article/view/3300https://doaj.org/toc/1121-760Xhttps://doaj.org/toc/2038-8306 The long non-coding FGD5-AS1 (LncFGD5-AS1) has been reported to be a novel carcinogenic gene and participant in regulating tumor progression by sponging microRNAs (miRNAs). However, the pattern of expression and the biological role of FGD5-AS1 in hepatocellular carcinoma (HCC) remains largely unknown. The expression level of FGD5-AS1 in tumor tissues and cell lines was measured by RT-qPCR. CCK-8, EdU, flow cytometry, wound healing, and transwell chamber assays were performed to investigate the role of FGD5-AS1 in cell proliferation, apoptosis, migration, and invasion in HCC. Dual luciferase reporter, and RNA pull-down assays were performed to identify the regulatory interactions among FGD5-AS1, miR-873-5p and GTP-binding protein 4 (GTPBP4). We found that the expression of FGD5-AS1 was upregulated in HCC tissues and cell lines. Moreover, the knockdown of FGD5-AS1 suppressed cell proliferation, migration and invasion, and induced apoptosis in HCC cells. Further studies demonstrated that FGD5-AS1 could function as a competitive RNA by sponging miR-873-5p in HCC cells. Moreover, GTPBP4 was identified as direct downstream target of miR-873-5p in HCC cells and FGD5-AS1mediated the effects of GTPBP4 by competitively binding with miR-873-5p. Taken together, this study demonstrated the regulatory role of FGD5-AS1 in the progression of HCC and identified the miR-873-5p/GTPBP4 axis as the direct downstream pathway. It represents a promising novel therapeutic strategy for HCC patients. Nuobei ZhangHao ShenShenan HuangFenfen WangHuifang LiuFen XieLei JiangXin ChenPAGEPress PublicationsarticleHepatocellular carcinomaFGD5-AS1miR-873-5pGTPBP4Biology (General)QH301-705.5ENEuropean Journal of Histochemistry , Vol 65, Iss 4 (2021) |
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Hepatocellular carcinoma FGD5-AS1 miR-873-5p GTPBP4 Biology (General) QH301-705.5 |
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Hepatocellular carcinoma FGD5-AS1 miR-873-5p GTPBP4 Biology (General) QH301-705.5 Nuobei Zhang Hao Shen Shenan Huang Fenfen Wang Huifang Liu Fen Xie Lei Jiang Xin Chen LncRNA FGD5-AS1 functions as an oncogene to upregulate GTPBP4 expression by sponging miR-873-5p in hepatocellular carcinoma |
description |
The long non-coding FGD5-AS1 (LncFGD5-AS1) has been reported to be a novel carcinogenic gene and participant in regulating tumor progression by sponging microRNAs (miRNAs). However, the pattern of expression and the biological role of FGD5-AS1 in hepatocellular carcinoma (HCC) remains largely unknown. The expression level of FGD5-AS1 in tumor tissues and cell lines was measured by RT-qPCR. CCK-8, EdU, flow cytometry, wound healing, and transwell chamber assays were performed to investigate the role of FGD5-AS1 in cell proliferation, apoptosis, migration, and invasion in HCC. Dual luciferase reporter, and RNA pull-down assays were performed to identify the regulatory interactions among FGD5-AS1, miR-873-5p and GTP-binding protein 4 (GTPBP4). We found that the expression of FGD5-AS1 was upregulated in HCC tissues and cell lines. Moreover, the knockdown of FGD5-AS1 suppressed cell proliferation, migration and invasion, and induced apoptosis in HCC cells. Further studies demonstrated that FGD5-AS1 could function as a competitive RNA by sponging miR-873-5p in HCC cells. Moreover, GTPBP4 was identified as direct downstream target of miR-873-5p in HCC cells and FGD5-AS1mediated the effects of GTPBP4 by competitively binding with miR-873-5p. Taken together, this study demonstrated the regulatory role of FGD5-AS1 in the progression of HCC and identified the miR-873-5p/GTPBP4 axis as the direct downstream pathway. It represents a promising novel therapeutic strategy for HCC patients.
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format |
article |
author |
Nuobei Zhang Hao Shen Shenan Huang Fenfen Wang Huifang Liu Fen Xie Lei Jiang Xin Chen |
author_facet |
Nuobei Zhang Hao Shen Shenan Huang Fenfen Wang Huifang Liu Fen Xie Lei Jiang Xin Chen |
author_sort |
Nuobei Zhang |
title |
LncRNA FGD5-AS1 functions as an oncogene to upregulate GTPBP4 expression by sponging miR-873-5p in hepatocellular carcinoma |
title_short |
LncRNA FGD5-AS1 functions as an oncogene to upregulate GTPBP4 expression by sponging miR-873-5p in hepatocellular carcinoma |
title_full |
LncRNA FGD5-AS1 functions as an oncogene to upregulate GTPBP4 expression by sponging miR-873-5p in hepatocellular carcinoma |
title_fullStr |
LncRNA FGD5-AS1 functions as an oncogene to upregulate GTPBP4 expression by sponging miR-873-5p in hepatocellular carcinoma |
title_full_unstemmed |
LncRNA FGD5-AS1 functions as an oncogene to upregulate GTPBP4 expression by sponging miR-873-5p in hepatocellular carcinoma |
title_sort |
lncrna fgd5-as1 functions as an oncogene to upregulate gtpbp4 expression by sponging mir-873-5p in hepatocellular carcinoma |
publisher |
PAGEPress Publications |
publishDate |
2021 |
url |
https://doaj.org/article/aba31fe3b7a944a5b44f019aa68d98ec |
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