Open AccessRETRACTED: Micro RNA ‐16 inhibits glioma cell growth and invasion through suppression of BCL 2 and the nuclear factor‐κB1/ MMP 9 signaling pathway
Author(s) -
Yang TianQuan,
Lu XiaoJun,
Wu TingFeng,
Ding DaDong,
Zhao ZhaoHui,
Chen GuiLin,
Xie XueShun,
Li Bin,
Wei YongXin,
Guo LingChuan,
Zhang Yu,
Huang YuLun,
Zhou YouXin,
Du ZiWei
Publication year - 2014
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.12351
Subject(s) - glioma , downregulation and upregulation , microrna , cancer research , u87 , biology , carcinogenesis , cell growth , apoptosis , cancer , gene , biochemistry , genetics
Recent studies have identified a class of small non‐coding RNA molecules, named micro RNA (mi RNA ), that is dysregulated in malignant brain glioblastoma. Substantial data have indicated that mi RNA ‐16 (miR‐16) plays a significant role in tumors of various origins. This mi RNA has been linked to various aspects of carcinogenesis, including cell apoptosis and migration. However, the molecular functions of miR‐16 in gliomagenesis are largely unknown. We have shown that the expression of miR‐16 in human brain glioma tissues was lower than in non‐cancerous brain tissues, and that the expression of miR‐16 decreased with increasing degrees of malignancy. Our data suggest that the expression of miR‐16 and nuclear factor ( NF )‐κB1 was negatively correlated with glioma levels. Micro RNA ‐16 decreased glioma malignancy by downregulating NF ‐κB1 and MMP 9, and led to suppressed invasiveness of human glioma cell lines SHG 44, U87, and U373. Our results also indicated that upregulation of miR‐16 promoted apoptosis by suppressing BCL 2 expression. Finally, the upregulation of miR‐16 in a nude mice model of human glioma resulted in significant suppression of glioma growth and invasiveness. Taken together, our experiments have validated the important role of miR‐16 as a tumor suppressor gene in glioma growth and invasiveness, and revealed a novel mechanism of miR‐16‐mediated regulation in glioma growth and invasiveness through inhibition of BCL 2 and the NF ‐κB1/ MMP ‐9 signaling pathway. Therefore, our experiments suggest the possible future use of miR‐16 as a therapeutic target in gliomas.