Long non coding RNA SLC26A4‐AS1 exerts antiangiogenic effects in human glioma by upregulating NPTX1 via NFKB1 transcriptional factor

Autor: Yiping Tang, Raoyu Yan, Shuang-Chun Liu, Weiqing Chen, Xiao-Fei Ding, Qunfeng Zhao, Jia-Ming Liu, Siye Lv, Ying Yu, Guang Chen, Haijun Li
Rok vydání: 2020
Předmět:
0301 basic medicine
Angiogenesis
Mice
Nude
Nerve Tissue Proteins
Biology
Biochemistry
Mice
03 medical and health sciences
0302 clinical medicine
Downregulation and upregulation
Cell Movement
Cell Line
Tumor
Glioma
otorhinolaryngologic diseases
medicine
Animals
Humans
Gene silencing
RNA
Small Interfering
Promoter Regions
Genetic
Molecular Biology
Transcription factor
Cell Proliferation
Regulation of gene expression
Mice
Inbred BALB C
Neovascularization
Pathologic
Brain Neoplasms
NF-kappa B p50 Subunit
Cell Biology
medicine.disease
NFKB1
Xenograft Model Antitumor Assays
Long non-coding RNA
Tumor Burden
Gene Expression Regulation
Neoplastic
C-Reactive Protein
030104 developmental biology
Sulfate Transporters
Case-Control Studies
030220 oncology & carcinogenesis
Cancer research
RNA
Long Noncoding
sense organs
Neoplasm Grading
Glioblastoma
Neuroglia
Signal Transduction
Zdroj: The FEBS Journal. 288:212-228
ISSN: 1742-4658
1742-464X
Popis: 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.
Databáze: OpenAIRE
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