Abstract
BackgroundGlioma is one prevalent malignant tumor originates from the central nervous system. Dysregulation of long non-coding RNAs (lncRNAs) has been found to be a molecular signature behind the pathology of a variety of cancers, including glioma. EIF3J antisense RNA 1 (EIF3J-AS1) is a novel lncRNA, whose performance in carcinogenesis has been unfolded. Nevertheless, the role of EIF3J-AS1 has never been investigated in glioma.MethodsqRT-PCR analysis was adopted to evaluate the relative levels of RNAs. In vitro functional assays, including colony formation, EdU, TUNEL and caspase-3/8/9 activity assays were conducted to study the impacts of EIF3J-AS1 on glioma. Dual-luciferase activity assays, RNA pull down assay and RIP assay were performed to elucidate molecular interplay among genes.ResultsEIF3J-AS1 was overexpressed in glioma cell lines. Knockdown of EIF3J-AS1 hampered glioma malignant phenotypes. MiR-1343-3p could bind to EIF3J-AS1. Moreover, miR-1343-3p targeted Annexin A11 (ANXA11) in its 3′UTR region. Mechanistically, EIF3J-AS1 relieved ANXA11 from miR-1343-3p silencing in the EIF3J-AS1/miR-1343-3p/ANXA11 RNA induced silencing complex (RISC), thus eliciting promoting effects on glioma progression. MiR-1343-3p inhibitor and ANXA11 overexpression offset the inhibitory impacts of EIF3J-AS1 silencing on glioma development.ConclusionEIF3J-AS1/miR-1343-3p/ANXA11 axis significantly affected biological behaviors in glioma, suggesting new therapeutic target for glioma treatment.
Highlights
Glioma is one prevalent malignant tumor originates from the central nervous system
Upregulation of EIF3J‐AS1 in glioma facilitates malignant progression of glioma To determine the possible role of EIF3J-AS1 in glioma, we evaluated its expression in 40 glioma samples with 10 normal brain tissues as control group
EIF3J-AS1 expression levels in glioma cell lines were distinctively higher than the normal HEB cell line (Fig. 1a)
Summary
Glioma is one prevalent malignant tumor originates from the central nervous system. Dysregulation of long non-coding RNAs (lncRNAs) has been found to be a molecular signature behind the pathology of a variety of cancers, including glioma. Numerous evidence have indicated that long non-coding RNAs (lncRNAs) played important part in regulating the development of human diseases, even the malignant progression of cancers, including glioma [6,7,8]. In the classical model of ceRNA network, lncRNAs that harbor miRNA-response elements (MREs) could sequester miRNAs and offset the repression effects on target messenger RNAs (mRNAs) [13]. This important regulatory mechanism of lncRNAs was gradually gaining increasing attention in anti-cancer research. LncRNA EIF3J antisense RNA 1 (EIF3J-AS1) was firstly reported to notably up-regulated in hepatocellular carcinoma (HCC) tumor samples and closely related with recurrence-free survival in HCC [15]. Its latent biological performance for glioma cells malignant behaviors has never been studied
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