Fan Zhang1, Zhongjun Wu2. 1. Department of Hepatobiliary Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. 2. Department of Hepatobiliary Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. Electronic address: yangce31@aol.com.
Abstract
PURPOSE: In this study, we assessed the expression and functions of microRNA-511-3p (miR-511-3p) in human prostate cancer (CaP). METHODS: Gene expressions of miR-511-3p in CaP cells and human CaP tumors were assessed by qPCR. In VCaP and PC3 cells, miR-511-3p was overexpressed by lentivirus. The functions of miR-511-3p upregulation in regulating in vitro cancer proliferation, migration and in vivo cancer growth were assessed by MTT, transwell and transplantation assays, respectively. Downstream target gene of miR-511-3p, AKT3, was verified by dual-luciferase activity and qPCR assays. AKT3 was then overexpressed in miR-511-3p-upregulated CaP cells to assess its functions in miR-511-3p-mediated cancer regulation. RESULTS: MiR-511-3p is significantly downregulated in CaP cell lines, and human CaP tumors. MiR-511-3p was further downregulated in T3/T4-staged CaP tumors and closely correlated with shorter overall survival among CaP patients. In VCaP and PC3 cells, lentiviral-induced miR-511-3p upregulation was acting as a tumor suppressor by inhibiting in vitro cancer proliferation, migration and in vivo transplantation. Human AKT3 gene was confirmed to be the downstream target of miR-511-3p in CaP. In miR-511-3p-upregulated VCaP and PC3 cells, forced-overexpression of AKT3 reversed the tumor suppressive effects of miR-511-3p in CaP. CONCLUSION: MiR-511-3p may serve as a prognostic factor and tumor suppressor in CaP, very likely through inverse regulation of its downstream target gene of AKT3.
PURPOSE: In this study, we assessed the expression and functions of microRNA-511-3p (miR-511-3p) in humanprostate cancer (CaP). METHODS: Gene expressions of miR-511-3p in CaP cells and humanCaP tumors were assessed by qPCR. In VCaP and PC3 cells, miR-511-3p was overexpressed by lentivirus. The functions of miR-511-3p upregulation in regulating in vitro cancer proliferation, migration and in vivo cancer growth were assessed by MTT, transwell and transplantation assays, respectively. Downstream target gene of miR-511-3p, AKT3, was verified by dual-luciferase activity and qPCR assays. AKT3 was then overexpressed in miR-511-3p-upregulated CaP cells to assess its functions in miR-511-3p-mediated cancer regulation. RESULTS: MiR-511-3p is significantly downregulated in CaP cell lines, and humanCaP tumors. MiR-511-3p was further downregulated in T3/T4-staged CaP tumors and closely correlated with shorter overall survival among CaP patients. In VCaP and PC3 cells, lentiviral-induced miR-511-3p upregulation was acting as a tumor suppressor by inhibiting in vitro cancer proliferation, migration and in vivo transplantation. HumanAKT3 gene was confirmed to be the downstream target of miR-511-3p in CaP. In miR-511-3p-upregulated VCaP and PC3 cells, forced-overexpression of AKT3 reversed the tumor suppressive effects of miR-511-3p in CaP. CONCLUSION: MiR-511-3p may serve as a prognostic factor and tumor suppressor in CaP, very likely through inverse regulation of its downstream target gene of AKT3.
Authors: Przemysław A Stempor; Dror Avni; Raya Leibowitz; Yechezkel Sidi; Maria Stępień; Tomasz Dzieciątkowski; Paula Dobosz Journal: Int J Mol Sci Date: 2021-03-04 Impact factor: 5.923