High expression of GALNT7 promotes invasion and proliferation of glioma cells

Shi, Hua; Li, Hongyan; Liu, Yuguang; Zhang, Jian; Cheng, Yanhao; Dai, Chao

doi:10.3892/ol.2018.9498

Cited by 14 publications

(18 citation statements)

References 47 publications

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“…Owing to rapid proliferation, metastasis and angiogenesis, this disease is relatively hard to treat (17,18). The prognosis of patients with glioma is relatively poor due to metastasis and recurrence (3,19). The incidence and mortality rates of glioma are continuously increasing (1).…”

Section: Discussionmentioning

confidence: 99%

“…Glioma is an aggressive brain cancer with high morbidity and mortality rates (1) characterized by aggressive proliferation, invasion and dismal prognosis (2). Although great progress has been made in the therapeutic field, the prognosis of patients with glioma remains poor (3). Recent studies have revealed a number of aberrantly expressed genes, which may be involved in the progression of glioma (4,5).…”

Section: Introductionmentioning

confidence: 99%

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Identification of differentially expressed microRNAs and the potential of microRNA‑455‑3p as a novel prognostic biomarker in glioma

Wang

Zhao³

et al. 2019

Oncol Lett

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Glioma is an aggressive central nervous system malignancy. MicroRNAs (miRNAs/miRs) have been reported to be involved in the tumorigenesis of numerous types of cancer, including glioma. The present study aimed to identify the differentially expressed miRNAs in glioma, and further explore the clinical value of miR-455-3p in patients with glioma. GEO2R was used for the identification of the differentially expressed miRNAs according to the miRNA expression profiles obtained from the Gene Expression Omnibus database. OncomiR was used to analyze the relationship of miRNAs with the survival outcomes of the patients with glioma. A total of 108 patients with glioma were recruited to examine the expression levels of miR-455-3p and further explore its clinical value. The bioinformatics analysis results suggested that a total of 64 and 48 differentially expressed miRNAs were identified in the GSE90603 and GSE103229 datasets, respectively. There were 12 miRNAs in the overlap of the two datasets, of which three were able to accurately predict overall cancer survival, namely hsa-miR-7-5p, hsa-miR-21-3p and hsa-miR-455-3p. In patients with glioma, miR-455-3p was determined to be significantly upregulated (P<0.001). Additionally, patients with high miR-455-3p expression had significantly lower 5-year overall survival than those with low miR-455-3p expression (log-rank test, P=0.001). Cox regression analysis further determined that miR-455-3p was an independent prognostic indicator for overall survival in patients with glioma (hazard ratio=2.136; 95% CI=1.177-3.877; P=0.013). In conclusion, the present study revealed a series of miRNAs with potential functional roles in the pathogenesis of glioma, and provides findings that indicate miR-455-3p as a promising biomarker for the prognosis of glioma.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Identification of differentially expressed microRNAs and the potential of microRNA‑455‑3p as a novel prognostic biomarker in glioma

Wang

Zhao³

et al. 2019

Oncol Lett

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“…Other potentially relevant genes displaying the same expression trend were the heparan sulphate proteoglycan GPC2 (a marker of immature neurons 62,63 ), the helix-loop-helix transcription factor ID4 (a marker of postmitotic neurons 64 ), and the signaling molecule FGFR3 that has been implicated in epilepsy 65 . Genes downregulated in KO cells and upregulated in rescue cells included urokinase-type plasminogen activator PLAU (deficiency in mouse models increases seizure susceptibility 66 ), the glycoprotein GALNT7 (upregulation of which has been found to promote glioma cell invasion 67 ) and the brain tumor gene MYBL1 (that has been shown to be regulated by O -linked N -acetylglucosamine 68 . Similar expression changes were observed in NSCs differentiated from induced pluripotent stem cells (iPSCs) that we had generated from family 1 ( Supplementary Figure 6) .…”

Section: Resultsmentioning

confidence: 99%

Loss of UGP2 in brain leads to a severe epileptic encephalopathy, emphasizing that bi-allelic isoform specific start-loss mutations of essential genes can cause genetic diseases

Perenthaler

Nikoncuk

Yousefi

et al. 2019

Preprint

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2 52 Running title: Loss of UGP2 causes a severe epileptic encephalopathy 53 54 55 Abstract: 60 Developmental and/or epileptic encephalopathies (DEEs) are a group of devastating genetic 61 disorders, resulting in early onset, therapy resistant seizures and developmental delay. Here we 62 report on 12 individuals from 10 families presenting with a severe form of intractable epilepsy, 63 severe developmental delay, progressive microcephaly and visual disturbance. Whole exome 64 sequencing identified a recurrent, homozygous variant (chr2:64083454A>G) in the essential UDP-65 glucose pyrophosphorylase (UGP2) gene in all probands. This rare variant results in a tolerable 66Met12Val missense change of the longer UGP2 protein isoform but causes a disruption of the start 67 codon of the shorter isoform. We show that the absence of the shorter isoform leads to a reduction 68 of functional UGP2 enzyme in brain cell types, leading to altered glycogen metabolism, upregulated 69unfolded protein response and premature neuronal differentiation, as modelled during pluripotent 70 stem cell differentiation in vitro. In contrast, the complete lack of all UGP2 isoforms leads to 71 differentiation defects in multiple lineages in human cells. Reduced expression of Ugp2a/Ugp2b in 72 vivo in zebrafish mimics visual disturbance and mutant animals show a behavioral phenotype. Our 73 study identifies a recurrent start codon mutation in UGP2 as a cause of a novel autosomal recessive 74 DEE. Importantly, it also shows that isoform specific start-loss mutations causing expression loss of a 75 tissue relevant isoform of an essential protein can cause a genetic disease, even when an organism-76 wide protein absence is incompatible with life. We provide additional examples where a similar 77 disease mechanism applies. 78 79 80 81 82 83 84 85 86 87 3 Introduction: 88 Developmental and/or epileptic encephalopathies (DEEs) are a heterogeneous group of genetic 89 disorders, characterized by severe epileptic seizures in combination with developmental delay or 90 regression 1 . Genes involved in multiple pathophysiological pathways have been implicated in DEEs, 91 including synaptic impairment, ion channel alterations, transporter defects and metabolic processes 92 such as disorders of glycosylation 2 . Mostly, dominant acting, de novo mutations have been identified 93 in children suffering from DEEs 3 , and only a limited number of genes with a recessive mode of 94 inheritance are known so far, with a higher occurrence rate in consanguineous populations 4 . A recent 95 cohort study on DEEs employing whole exome sequencing (WES) and copy-number analysis, 96however, found that up to 38% of diagnosed cases might be caused by recessive genes, indicating 97 that the importance of this mode of inheritance in DEEs has been underestimated 5 . 98

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“…For example, CSGALNACT1 is implicated mostly in prostate cancer, but also serves as a prognostic biomarker in multiple myeloma (Qi et al 2020). GALNT7 is favorable as a prognostic biomarker in colorectal cancer and gliomas, but has unfavorable results in pancreatic cancer with a lower survival rate [https://www.proteinatlas.org] (Uhlen et al 2015; Hua et al 2018). STT3A has also been recognized as a diagnostic panel biomarker for thyroid cancer, and ALG10 autoantibodies have been implicated as potential diagnostic biomarkers for breast cancer, consistent with the data in EDRN (Zhong et al 2008).…”

Section: Discussionmentioning

confidence: 99%

Differential expression of glycosyltransferases identified through comprehensive pan-cancer analysis

Vora

Cauley

et al. 2021

Preprint

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Despite accumulating evidence supporting a role for glycosylation in cancer progression and prognosis, the complexity of the human glycome and glycoproteome poses many challenges to understanding glycosylation-related events in cancer. In this study, a multifaceted genomics approach was applied to analyze the impact of differential expression of glycosyltransferases (GTs) in 16 cancers. An enzyme list was compiled and curated from numerous resources to create a consensus set of GTs. Resulting enzymes were analyzed for differential expression in cancer, and findings were integrated with experimental evidence from other analyses, including: similarity of healthy expression patterns across orthologous genes, miRNA expression, automatically-mined literature, curation of known cancer biomarkers, N-glycosylation impact, and survival analysis. The resulting list of GTs comprises 222 human enzymes based on annotations from five databases, 84 of which were differentially expressed in more than five cancers, and 14 of which were observed with the same direction of expression change across all implicated cancers. 25 high-value GT candidates were identified by cross-referencing multimodal analysis results, including PYGM, FUT6 and additional fucosyltransferases, several UDP-glucuronosyltransferases, and others, and are suggested for prioritization in future cancer biomarker studies. Relevant findings are available through OncoMX at https://data.oncomx.org, and the overarching pipeline can be used as a framework for similarly analysis across diverse evidence types in cancer. This work is expected to improve the understanding of glycosylation in cancer by transparently defining the space of glycosyltransferase enzymes and harmonizing variable experimental data to enable improved generation of data-driven cancer biomarker hypotheses.

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High expression of GALNT7 promotes invasion and proliferation of glioma cells

Cited by 14 publications

References 47 publications

Identification of differentially expressed microRNAs and the potential of microRNA‑455‑3p as a novel prognostic biomarker in glioma

Identification of differentially expressed microRNAs and the potential of microRNA‑455‑3p as a novel prognostic biomarker in glioma

Loss of UGP2 in brain leads to a severe epileptic encephalopathy, emphasizing that bi-allelic isoform specific start-loss mutations of essential genes can cause genetic diseases

Differential expression of glycosyltransferases identified through comprehensive pan-cancer analysis

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