ABAT targeted by miR-183-5p regulates cell functions in liver cancer

Liver cancer triggers a considerable number of global deaths. This work focused on mechanisms as well as impacts of ABAT in liver cancer. Differentially expressed mRNAs in liver cancer were analyzed with The Cancer Genome Atlas (TCGA) database to determine and evaluate the prognostic significance of...

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Veröffentlicht in:The international journal of biochemistry & cell biology 2021-12, Vol.141, p.106116, Article 106116
Hauptverfasser: Han, Hui, Zhou, Shenkang, Chen, Gengzhen, Lu, Yandi, Lin, Hui
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container_title The international journal of biochemistry & cell biology
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creator Han, Hui
Zhou, Shenkang
Chen, Gengzhen
Lu, Yandi
Lin, Hui
description Liver cancer triggers a considerable number of global deaths. This work focused on mechanisms as well as impacts of ABAT in liver cancer. Differentially expressed mRNAs in liver cancer were analyzed with The Cancer Genome Atlas (TCGA) database to determine and evaluate the prognostic significance of the target gene ABAT. ABAT was overexpressed to explore its effect on liver cancer. Furthermore, the targeted regulation between miR-183-5p and ABAT was verified through dual-luciferase method. The effects of their expression on liver cancer functions were detected by cell functional experiments like Cell Counting Kit-8 (CCK8), Transwell and flow cytometry. Lastly, the inhibitory effect of ABAT on the tumor was proved in nude mice in vivo. At tissue and cell levels, ABAT was inactivated in liver cancer, and liver cancer patients with lowly expressed ABAT had poor prognosis. Overexpressing ABAT could inhibit cancer cell behaviors, and suppress tumorigenesis in nude mice. Meanwhile, overexpressed ABAT could upregulate E-cadherin in liver cancer cells, while downregulate MMP-9, Vimentin, MMP-2, N-cadherin, Ki67. Of note, miR-183-5p was highly expressed in liver cancer tissue and cells, which could target and downregulate ABAT expression. It was indicated by rescue assay that lowly expressed miR-183-5p could repress functions of liver cancer cells, while such inhibitory effect could be recovered by ABAT silencing. Downstream of miR-183-5p, ABAT was targeted to mediate progression of liver cancer. •High ABAT level could inhibit the proliferation, migration and invasion of liver cancer cells.•ABAT could be targeted and downregulated by miR-183-5p.•Low miR-183-5p level could inhibit the proliferation, migration and invasion of liver cancer cells.•MiR-183-5p could target and regulate ABAT to regulate the malignant progression of liver cancer.
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This work focused on mechanisms as well as impacts of ABAT in liver cancer. Differentially expressed mRNAs in liver cancer were analyzed with The Cancer Genome Atlas (TCGA) database to determine and evaluate the prognostic significance of the target gene ABAT. ABAT was overexpressed to explore its effect on liver cancer. Furthermore, the targeted regulation between miR-183-5p and ABAT was verified through dual-luciferase method. The effects of their expression on liver cancer functions were detected by cell functional experiments like Cell Counting Kit-8 (CCK8), Transwell and flow cytometry. Lastly, the inhibitory effect of ABAT on the tumor was proved in nude mice in vivo. At tissue and cell levels, ABAT was inactivated in liver cancer, and liver cancer patients with lowly expressed ABAT had poor prognosis. Overexpressing ABAT could inhibit cancer cell behaviors, and suppress tumorigenesis in nude mice. Meanwhile, overexpressed ABAT could upregulate E-cadherin in liver cancer cells, while downregulate MMP-9, Vimentin, MMP-2, N-cadherin, Ki67. Of note, miR-183-5p was highly expressed in liver cancer tissue and cells, which could target and downregulate ABAT expression. It was indicated by rescue assay that lowly expressed miR-183-5p could repress functions of liver cancer cells, while such inhibitory effect could be recovered by ABAT silencing. Downstream of miR-183-5p, ABAT was targeted to mediate progression of liver cancer. •High ABAT level could inhibit the proliferation, migration and invasion of liver cancer cells.•ABAT could be targeted and downregulated by miR-183-5p.•Low miR-183-5p level could inhibit the proliferation, migration and invasion of liver cancer cells.•MiR-183-5p could target and regulate ABAT to regulate the malignant progression of liver cancer.</description><identifier>ISSN: 1357-2725</identifier><identifier>ISSN: 1878-5875</identifier><identifier>EISSN: 1878-5875</identifier><identifier>DOI: 10.1016/j.biocel.2021.106116</identifier><identifier>PMID: 34742920</identifier><language>eng</language><publisher>Netherlands: Elsevier Ltd</publisher><subject>ABAT ; Animals ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Proliferation - genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Invasion ; Liver cancer ; Liver Neoplasms - genetics ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Migration ; MiR-183-5p ; Proliferation</subject><ispartof>The international journal of biochemistry &amp; cell biology, 2021-12, Vol.141, p.106116, Article 106116</ispartof><rights>2021 Elsevier Ltd</rights><rights>Copyright © 2021 Elsevier Ltd. 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Meanwhile, overexpressed ABAT could upregulate E-cadherin in liver cancer cells, while downregulate MMP-9, Vimentin, MMP-2, N-cadherin, Ki67. Of note, miR-183-5p was highly expressed in liver cancer tissue and cells, which could target and downregulate ABAT expression. It was indicated by rescue assay that lowly expressed miR-183-5p could repress functions of liver cancer cells, while such inhibitory effect could be recovered by ABAT silencing. 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subjects ABAT
Animals
Cell Line, Tumor
Cell Movement - genetics
Cell Proliferation - genetics
Female
Gene Expression Regulation, Neoplastic
Humans
Invasion
Liver cancer
Liver Neoplasms - genetics
Liver Neoplasms - metabolism
Liver Neoplasms - pathology
Male
Mice
Mice, Inbred BALB C
Mice, Nude
MicroRNAs - genetics
MicroRNAs - metabolism
Migration
MiR-183-5p
Proliferation
title ABAT targeted by miR-183-5p regulates cell functions in liver cancer
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