background: Liver cancer triggers a considerable number of global deaths. This work focused on mechanisms as well as impacts of ABAT in liver cancer.
methods: 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 ... More
background: Liver cancer triggers a considerable number of global deaths. This work focused on mechanisms as well as impacts of ABAT in liver cancer.
methods: 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.
results: 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.
conclusions: Downstream of miR-183-5p, ABAT was targeted to mediate progression of liver cancer.
