Abstract
Objectives: Gliomas remain one of serious public health problems worldwide which demand further and deeper investigation. The aim of this study was to explore the association between synapse defective protein 1 homolog 1 (SYDE1) and gliomas via public database analysis and in vitro validation to determine the potential diagnostic and prognostic values. Methods and Results: Compared with healthy brain tissues, there was a significant increase in SYDE1 expression in glioma tissues. Additionally, SYDE1 exhibited higher expression levels in glioma patients with unfavorable clinicopathological factors. In vitro knockdown of SYDE1 in glioma cell lines A172 inhibited their migrative and invasive ability but not the proliferative ability. GO and KEGG pathway analysis of the top 100 genes coexpressed with SYDE1 showed enrichments of tumor-associated terms. Further bioinformatic analysis revealed that the SNHG16/hsa-miR-520e/SYDE1 axis might be involved in glioma development. Conclusions: SYDE1 is expressed at higher levels in gliomas than in healthy brains, and can promote metastasis and invasion but not proliferation of gliomas. Furthermore, SYDE1 has values in the diagnosis and prognosis prediction of gliomas.
Highlights
Gliomas are one of the most common invasive malignancies in the central nervous system, accounting for approximately 51.4% of all primary brain tumors (Xue et al, 2017)
We utilized publicly available data from the Oncomine, Gene expression profiling interactive analysis 2 (GEPIA2) and Human Protein Atlas (HPA) databases to examine SYDE1 expression in glioma tissues and normal control tissues, and we identified an increased level of SYDE1 in gliomas
The GEPIA2 databases indicated that SYDE1 was expressed at higher levels in glioma subclasses LGG and GBMs than in the corresponding normal tissues (p < 0.05, Figure 1C)
Summary
Gliomas are one of the most common invasive malignancies in the central nervous system, accounting for approximately 51.4% of all primary brain tumors (Xue et al, 2017). According to the 2007 WHO classification of central nervous system tumors, gliomas can be divided into low-grade glioma (LGG, grade I and II) and high-grade glioma (HGG, grade III and IV) (Louis et al, 2007). This classification is mainly based on the clinical and histopathological features of the glioma. Given that IDH mutations and 1p/19q codeletions occur mostly in different subtypes of gliomas, the 2016 edition of the WHO glioma classification faces great challenges in clinical practice. It is of great necessity to acquire an in-depth understanding of gliomas and identify other causal genes
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