MiR-15b/HOTAIR/p53 form a regulatory loop that affects the growth of glioma cells.

Among the malignant tumors of the human central nervous system, gliomas have the highest incidence and recurrence rate. Therefore, exploration of the molecular mechanism that underlies the development and progression of gliomas is of great clinical significance. Many studies have demonstrated that long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) play important roles in the development and progression of tumors. In the present study, both an RNAhybrid analysis and a dual-luciferase reporter gene assay confirmed that microRNA-15b (miR-15b) binding sites were present in the sequence of HOX transcript antisense RNA (HOTAIR). The present study further demonstrated that miR-15b, HOTAIR, and p53 formed a mutually regulated loop. MiR-15b upregulated the expression of p53 but inhibited the expression of HOTAIR. In addition, miR-15b was able to regulate the expression of HOTAIR through p53. P53 promoted miR-15b expression but inhibited HOTAIR expression. Furthermore, the examination of cell proliferation, apoptosis, and invasion revealed that both miR-15b and p53 inhibited the proliferation and invasion, but promoted the apoptosis, of glioma cells. In contrast, HOTAIR exerted effects that were the opposite of those exerted by miR-15b and p53 on glioma cells. The upregulation of HOTAIR suppressed the inhibitory effects of miR-15b and p53 on cell proliferation and invasion as well as the promoting effect of miR-15b and p53 on apoptosis. Therefore, it can be concluded that miR-15b, HOTAIR, and p53 constitute a regulatory loop that is capable of regulating the growth of glioma cells. This finding provides a new target for the treatment of gliomas.

Sun G ，Wang Y ，Zhang J ，Lin N ，You Y ... -  《-》

Long noncoding RNA DLX6-AS1 accelerates the glioma carcinogenesis by competing endogenous sponging miR-197-5p to relieve E2F1.

Long noncoding RNAs (lncRNAs) participate in numerous of human cancer tumorigenesis. Nevertheless, the in-depth molecular mechanism that lncRNAs regulate the gliomagenesis is still ambiguous. In this research, our study invests energy in the biologic roles of lncRNA DLX6-AS1 on the glioma tumorigenesis. Here, we demonstrated that DLX6-AS1 expression was both high-expressed in the glioma cells and tissue, and the overexpression of DLX6-AS1 was clinically correlated with the poor outcome of glioma patients. In the cellular functional assays, silenced DLX6-AS1 expression by siRNAs inhibited the proliferation, invasion and tumor growth in vitro and in vivo, while the enhanced DLX6-AS1 expression by plasmids promotes them. The bioinformatics predictive tools, luciferase reporter assay and correlation analysis found that miR-197-5p could both target the 3'-UTR of DLX6-AS1 as well as E2F1 gene, constructing DLX6-AS1-miR-197-5p-E2F1 axis. Moreover, receiver operating characteristic (ROC) curve analysis revealed that lncRNA DLX6-AS1 has valuable diagnostic value clinical diagnose for the glioma patients (AUC = 0.736). Overall, our finding supports that DLX6-AS1 accelerates the glioma carcinogenesis by competing endogenous sponging miR-197-5p to relieve E2F1, acting as a novel therapeutic target for glioma.

Li X ，Zhang H ，Wu X 《-》

The Long Noncoding RNA TP73-AS1 Interacted with miR-124 to Modulate Glioma Growth by Targeting Inhibitor of Apoptosis-Stimulating Protein of p53.

Xiao S ，Wang R ，Wu X ，Liu W ，Ma S ... -  《-》

Knockdown of long non-coding RNA HOTAIR inhibits malignant biological behaviors of human glioma cells via modulation of miR-326.

Ke J ，Yao YL ，Zheng J ，Wang P ，Liu YH ，Ma J ，Li Z ，Liu XB ，Li ZQ ，Wang ZH ，Xue YX ... -  《Oncotarget》

Long non-coding RNA HOTAIR acts as a competing endogenous RNA to promote glioma progression by sponging miR-126-5p.

LncRNA HOX transcript antisense intergenic RNA (HOTAIR) has been shown to play prominent roles in tumorigenesis. However, its precise molecular mechanism in glioma has not been completely elucidated. In this study, we found that HOTAIR was aberrantly up-regulated in glioma tissues and was negatively correlated with miR-126-5p expression. Next, we determined that HOTAIR promote glioma progression by sponging miR-126-5p. Subsequently, glutaminase (GLS) was confirmed to be a direct target of miR-126-5p using bioinformatics software and a luciferase reporter assay. Moreover, HOTAIR could modulate GLS expression by functioning as a competing endogenous RNA (ceRNA) for miR-126-5p. Taken together, our study clarified that the HOTAIR/miR-126/GLS pathway is involved in glioma progression and may potentially serve as a target for glioma therapy.

Liu L ，Cui S ，Wan T ，Li X ，Tian W ，Zhang R ，Luo L ，Shi Y ... -  《-》