caa a22 4500 606233695 CHVBK 20210128101233.0 cr unu---uuuuu 210128e20150601xx s 000 0 eng 10.1007/s11010-015-2382-6 doi (NATIONALLICENCE)springer-10.1007/s11010-015-2382-6 MiR-129-2 functions as a tumor suppressor in glioma cells by targeting HMGB1 and is down-regulated by DNA methylation [Elektronische Daten] [Yu Yang, Jun-Qiang Huang, Xi Zhang, Liang-Fang Shen] MicroRNA (miRNA) dysregulation is causally related to cancer development and progression, and recent reports have revealed that DNA methylation constitutes an important mechanism for miRNA deregulation in cancer. MiR-129-2 has been reported to be down-regulated and functions as a tumor suppressor in a few human cancers. However, the involvement of miR-129-2 in the pathology of glioma and the mechanism underlying miR-129-2 regulation in glioma cells remain unclear. In this study, we performed quantitative PCR to investigate the level of miR-129-2 in 21 pairs of glioma tumors and matched adjacent tissues and found that miR-129-2 is down-regulated in glioma tumors. In vitro cell growth, apoptosis, cell migration, and invasion assays revealed that miR-129-2 functions as a tumor suppressor in glioma cells. Luciferase reporter assay found that miR-129-2 could directly target high-mobility group box 1 (HMGB1) and inhibit its expression in glioma cells. Methylation-specific PCR found that DNA methylation in upstream regions of miR-129-2 occured more frequently in cancer tissues than in adjacent tissues. Demethylation of miR-129-2 by 5-aza-2′-deoxycytidine treatment and quantitative PCR analysis revealed that miR-129-2 expression is epigenetically regulated in glioma cells. Taken together, our data suggested that miR-129-2 functions as a tumor suppressor in glioma cells by directly targeting HMGB1 and is down-regulated by DNA methylation, which may provide a novel therapeutic strategy for treatment of glioma. The Author(s), 2015 Glioma nationallicence miR-129-2 nationallicence High-mobility group box 1 nationallicence DNA methylation nationallicence Yang Yu Department of Oncology, Xiangya Hospital, Central South University, 410008, Changsha, Hunan, China aut Huang Jun-Qiang Department of Neurosurgery, The First Hospital of Changsha, 430100, Changsha, China aut Zhang Xi Department of Oncology, The Third Xiangya Hospital, Central South University, 430100, Changsha, China aut Shen Liang-Fang Department of Oncology, Xiangya Hospital, Central South University, 410008, Changsha, Hunan, China aut Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 404/1-2(2015-06-01), 229-239 0300-8177 404:1-2<229 2015 404 11010 https://doi.org/10.1007/s11010-015-2382-6 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s11010-015-2382-6 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Yang Yu Department of Oncology, Xiangya Hospital, Central South University, 410008, Changsha, Hunan, China aut NATIONALLICENCE 700 1- Huang Jun-Qiang Department of Neurosurgery, The First Hospital of Changsha, 430100, Changsha, China aut NATIONALLICENCE 700 1- Zhang Xi Department of Oncology, The Third Xiangya Hospital, Central South University, 430100, Changsha, China aut NATIONALLICENCE 700 1- Shen Liang-Fang Department of Oncology, Xiangya Hospital, Central South University, 410008, Changsha, Hunan, China aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 404/1-2(2015-06-01), 229-239 0300-8177 404:1-2<229 2015 404 11010