Exosomal lncRNA‑ATB activates astrocytes that promote glioma cell invasion.

Glioma invasion is a main cause of a poor prognosis and relapse in patients suffering from the disease. However, the molecular mechanisms responsible for glioma cell invasion remain poorly understood. In this study, the characteristics of exosomes were identified using electron microscope (TEM), and western blot analysis.

Long non-coding RNA SPRY4-IT1 promotes the proliferation and invasion of U251 cells through upregulation of SKA2.

The long non-coding RNA SPRY4-intronic transcript 1 (SPRY4-IT1) has been shown to promote the progression of cancer; however, the role of SPRY4-IT1 in glioma remains unclear. The present study demonstrated that SPRY4-IT1 expression was markedly increased in glioma tissues and cells compared with normal brain tissues, whereas knockdown of SPRY4-IT1 inhibited cell proliferation, migration, and invasion in U251 cells. Spindle and kinetochore associated complex subunit 2 (SKA2) was found to be a target of SPRY4-IT1 and was downregulated by SPRY4-IT1-knockdown.

TGF-β-mediated repression of MST1 by DNMT1 promotes glioma malignancy.

Human gliomas are related to high rates of morbidity and mortality. TGF-β promotes the growth of glioma cells, and correlate with the degree of malignancy of human gliomas. However, the molecular mechanisms involved in the malignant function of TGF-β are not fully elucidated.

Long non-coding RNA ATB promotes glioma malignancy by negatively regulating miR-200a.

Background: Glioma is one of the most common and aggressive primary malignant tumor in the brain. Accumulating evidences indicated that aberrantly expressed non-coding RNAs (ncRNAs), including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), contribute to tumorigenesis. However, potential mechanisms between lncRNAs and miRNAs in glioma remain largely unknown.

Epigenetic modification of miR-141 regulates SKA2 by an endogenous 'sponge' HOTAIR in glioma.

Aberrant expression of miR-141 has recently implicated in the occurrence and development of various types of malignant tumors. However whether the involvement of miR-141 in the pathogenesis of glioma remains unknown. Here, we showed that miR-141 was markedly downregulated in glioma tissues and cell lines compared with normal brain tissues, and its expression correlated with the pathological grading.

Epigenetic repression of long non-coding RNA MEG3 mediated by DNMT1 represses the p53 pathway in gliomas.

Epigenetic regulation plays a significant role in gliomas. However, how methylation and long non-coding RNA (lncRNA) cooperates to regulate gliomas progression is largely unknown. In this investigation we showed that the downregulation of MEG3 expression due to hypermethylation of MEG3 was observed in gliomas tissues.