Abstract
Glioblastoma (GBM), the primary malignant brain tumor, is typically associated with a poor prognosis and poor quality of life, mainly due to the lack of early diagnostic biomarkers and therapeutic targets. However, gene sequencing technologies and bioinformatics analysis are currently being actively utilized to explore potential targets for the diagnosis and management of malignancy. Herein, based on a variety of bioinformatics tools for the reverse prediction of target genes associated with the prognosis of GBM, a ceRNA network of AGAP2-AS1-miR-9-5p-MMP2/MMP9 was constructed, and a potential therapeutic target for GBM was identified. Enrichment analysis predicted that the ceRNA regulatory network participates in the processes of cell proliferation, differentiation, and migration.
Highlights
Glioblastoma (GBM) is the most common malignant primary brain tumor in the central nervous system (CNS) [1]
For cell components (CC), upregulated differentially expressed genes (DEGs) were mainly enriched in the collagen-containing extracellular matrix, endoplasmic reticulum lumen, and secretory granule lumen; downregulated DEGs were mainly enriched in presynapse, synaptic membrane, and neuronal cell body
For molecular function (MF), upregulated DEGs were mainly enriched in extracellular matrix structural constituents, cell adhesion molecule binding, and peptidase regulator activity; downregulated DEGs were mainly enriched in metal ion transmembrane transporter activity, channel activity, and passive transmembrane transporter activity
Summary
Glioblastoma (GBM) is the most common malignant primary brain tumor in the central nervous system (CNS) [1]. The progressive decline in neurological function and quality of life that results from GBM could have a devastating impact on patients themselves as well as their caregivers and families [3]. An increasing number of studies have reported that non-coding RNA (ncRNA) might play a significant role in pathologic processes, including tumorigenesis and the development of multiple malignant tumors [4]. There is a hypothesis that the competing endogenous RNA (ceRNA) holds that the long non-coding RNAs (lncRNAs) can sponge and inactivate microRNAs (miRNAs) that would otherwise target specific mRNAs for degradation or translational silencing, affecting the encoding of proteins [5]. By acting as miRNA sponges, lncRNAs regulate the expression levels of the targeted mRNAs, thereby affecting the biological behavior and pathologic process of cancer cells.
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