Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been reported that glioma has a higher morbidity and mortality than other types of malignant brain tumor. While glioma has been extensively researched, the exact molecular mechanisms of its genesis and progression have remained to be fully elucidated. In order to explore a novel glioma-associated pathway which may represent a therapeutic target, 61 pairs of tumor tissues and adjacent normal tissues of glioma patients were collected and subjected to reverse-transcription quantitative polymerase chain reaction analysis, indicating that the relative expression of microRNA (miR)-128-3p was significantly decreased in the tumor tissues. However, the expression of neuronal pentraxin 1 (NPTX1) was obviously elevated. Through a bioinformatics analysis using Targetscan and transfection experiments, it was confirmed that NPTX1 was targeted by miR-128-3p. In the U251 human glioma cell line, transfection with miR-128-3p mimics increased the levels of phosphorylated insulin receptor substrate 1 (p-IRS-1), phosphoinositide-3 kinase (PI3K) and p-AKT, as demonstrated by western blot analysis. In addition, the proliferation rate of the cells was notably decreased following transfection with miR-128-3p mimics. Conversely, transfection with miR-128-3p inhibitor significantly increased the levels of p-IRS-1, PI3K and p-AKT, accompanied by an elevated proliferation rate of the cells. Therefore, it was indicated that miR-128-3p could reversely regulate NPTX1 expression. After the expression of NPTX1 was inhibited with specific small interfering RNA, the levels of p-IRS-1, PI3K and p-AKT were obviously decreased, while the expression of miR-128-3p was not significantly changed. Overall, it was concluded that miR-128-3p suppresses glioma through the NPTX1/IRS-1/PI3K/AKT signaling pathway.
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PMID:miR-128-3p inhibits glioma cell proliferation and differentiation by targeting NPTX1 through IRS-1/PI3K/AKT signaling pathway. 3090 75

Malignant gliomas are a heterogeneous group of brain tumors with a poor prognosis, which is largely due to its aggressive invasiveness and angiogenesis. In recent years, it has been found that multiple long noncoding RNAs (lncRNAs) participate in a wide range of biological functions including angiogenesis through the regulation of gene expression in cancers. In this study, we investigate and report the novel role of lncRNA SLC26A4-AS1 in gliomas, with a novel mechanism involving transcription factors NFKB1 and NPTX1. We determined that SLC26A4-AS1 was downregulated in human glioma tissues and cells. Furthermore, overexpression of SLC26A4-AS1 or NPTX1 restrained the aggressiveness of glioma cells and their pro-angiogenic ability. SLC26A4-AS1 was also found to upregulate NPTX1 by recruiting NFKB1 into the NPTX1 promoter. Moreover, silencing of either NPTX1 or NFKB1 restored the aggressive and pro-angiogenic properties of glioma cells in the presence of SLC26A4-AS1. Taken together, we demonstrate that SLC26A4-AS1 promotes NPTX1 transcriptional activity by recruiting NFKB1 and thus exerting antiangiogenic effects on glioma cells. This study provides an experimental basis for the intervention of SLC26A4-AS1 in the treatment of gliomas.
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PMID:Long non coding RNA SLC26A4-AS1 exerts antiangiogenic effects in human glioma by upregulating NPTX1 via NFKB1 transcriptional factor. 3225 52