分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

AC016405.3, a novel long noncoding RNA, acts as a tumor suppressor through modulation of TET2 by microRNA-19a-5p sponging in glioblastoma

Siyang Ren, Yinghui Xu

Journal:CANCER SCIENCE

IF:4.75

DOI:10.1111/cas.14002

PMID:30888082

Published:2019-03-19

research field:

Abstract

Long non-coding RNAs (lncRNAs) are crucial regulators in various malignancies including glioblastoma multiforme (GBM). In the present study, we screened out a new lncRNA, AC016405.3, through a previous genome-wide lncRNA microarray analysis in GBM. It showed that AC016405.3 was downregulated in GBM tissue specimens and cell lines, and it also illustrated that the downregulated AC016405.3 was closely correlated with several aggressive features of patients with GBM. Functionally, we found that overexpression of AC016405.3 suppressed GBM cells’ proliferation and metastasis using a gain of function experiment. We further showed that microRNA (miR)-19a-5p, a carcinogenic miRNA, was a downstream miRNA of AC016405.3. AC016405.3 was revealed as a target of miR-19a-5p, and overexpression of miR-19a-5p reversed the inhibitive effect of AC016405.3 on GBM cell proliferation and metastasis. Furthermore, a novel downstream gene of miR-19a-5p, TET2 , was identified through a constructed microarray analysis. We showed that TET2 was downregulated in GBM and was involved in miR-19a-5p-mediated proliferation and metastasis by directly being targeted. Finally, through a western blot assay and a series of functional CCK-8 and metastatic assays, we showed that AC016405.3 suppressed proliferation and metastasis through modulation of TET2 by sponging of miR-19a-5p in GBM cells. In summary, the findings of the current study identified a novel lncRNA and illustrated that AC016405.3, acting as an anti-oncogene, suppressed GBM cell proliferation and metastasis by regulating TET through miR-19a-5p sponging. Our present study might provide a new axis in the molecular treatment of GBM.

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