期刊
MOLECULAR THERAPY-NUCLEIC ACIDS
卷 19, 期 -, 页码 905-921出版社
CELL PRESS
DOI: 10.1016/j.omtn.2019.10.043
关键词
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资金
- Natural Science Foundation of China [81872073, 81672511, 81872503, 81573010]
- Liaoning Science and Technology Plan Project [2017225020, 2015225007]
- Project of Key Laboratory of Neuro-oncology in Liaoning Province [112-2400017005]
- central government of Liaoning Province [2017011553-301]
- outstanding scientific fund of Shengjing Hospital [201304]
Glioblastomas are the most common and malignant intracranial tumors with a low survival rate. Dysregulation of long non-coding RNAs and RNA-binding protein causes various diseases, including cancers. However, the function of LINC00680 and TTN-AS1 in the progression of glioblastomas is still elusive. In this study, we detected that LINC00680 and TTN-AS1 were upregulated in glioblastoma cells. RNA-binding protein EIF4A3 could prolong the half-life of LINC00680 and TTNAS1. Knockdown of EIF4A3, LINC00680, and TTN-AS1 impaired proliferation, migration, and invasion and inhibited the growth of tumor in vivo and promoted apoptosis of glioblastoma cells. miR-320b was proven to be a target of LINC00680 and TTN-AS1. They interacted with miR-320b as competing endogenous RNAs, which resulted in the reduction of binding between transcriptional factor EGR3 (early growth response 3) mRNA and miR-320b. The accumulation of EGR3 promoted expression of plakophilin (PKP)2, which could activate the epidermal growth factor receptor (EFGR) pathway, leading to the malignant biological behaviors of glioblastoma cells. In summary, LINC00680 and TTN-AS1 promoted glioblastoma cell malignant biological behaviors via the miR-320b/EGR3/PKP2 axis by being stabilized by EIF4A3, which may provide a novel strategy for glioblastoma therapy.
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