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Last update 08 May 2025

MFNG

Last update 08 May 2025

Basic Info

Synonyms

Beta-1,3-N-acetylglucosaminyltransferase manic fringe, MFNG, MFNG O-fucosylpeptide 3-beta-N-acetylglucosaminyltransferase

+ [1]

Introduction

Glycosyltransferase that initiates the elongation of O-linked fucose residues attached to EGF-like repeats in the extracellular domain of Notch molecules (By similarity). Modulates NOTCH1 activity by modifying O-fucose residues at specific EGF-like domains resulting in inhibition of NOTCH1 activation by JAG1 and enhancement of NOTCH1 activation by DLL1 via an increase in its binding to DLL1 (By similarity).

Drugs associated with MFNG

HG-1064

Target

MFNG

Mechanism

MFNG modulators

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MFNG

100 Translational Medicine associated with MFNG

0 Patents (Medical) associated with MFNG

Literatures (Medical) associated with MFNG

01 Jan 2025·Journal of Molecular Medicine

Manic Fringe promotes endothelial-to-mesenchymal transition mediated by the Notch signalling pathway during heart valve development

Article

Author: Yang, Junjie ; Qin, Xiji ; Xu, Zhikang ; Wang, Jian ; Wang, Qingjie ; Zhou, Yue ; Wang, Yu ; Zuo, Mengying ; Sun, Kun ; Meng, Zhuo ; Wang, Zhi ; Chen, Sun ; Jiang, Shiwei

A fundamental event in the formation of heart valves involves the transformation of endocardial cells within the outflow tract (OFT) and atrioventricular canal (AVC) cushions through a process known as endothelial-to-mesenchymal transition (EndMT). Aberrant EndMT is a primary cause of congenital valvular malformations. Manic Fringe (MFNG) has been previously associated with cardiovascular development, although its role in heart valve development remains underexplored. In this study, we seek to enhance our understanding of MFNG's involvement in valve formation and its association with EndMT. Staining results of histological section revealed the expression of MFNG in the AVC and OFT from embryonic day 9.5 to 10.5 (E9.5-E10.5), when EndMT takes place. Cellular data demonstrated that MFNG exerts a positive regulatory influence on the EndMT process, promoting endothelial cell (EC) migration by enhancing the activity of the Notch signalling pathway. MFNG knockdown mediated by antisense morpholino oligonucleotides (MO) injection caused abnormal development of the heart and valves in zebrafish. Furthermore, through whole-exome sequencing (WES), we identified a heterozygous MFNG mutation in patients diagnosed with tetralogy of Fallot-pulmonary valve stenosis (TOF-PS). Cellular and molecular assays confirmed that this deleterious mutation reduced MFNG expression and hindered the EndMT process. In summary, our study verifies that MFNG plays a role in promoting EndMT mediated by the Notch signalling pathway during the heart and valve development. The MFNG deleterious variant induces MFNG loss of function, potentially elucidating the underlying molecular mechanisms of MFNG's involvement in the pathogenesis of congenital heart valve defects. These observations contribute to our current genetic understanding of congenital heart valve disease and may provide a potential target for prenatal diagnosis and treatment. KEY MESSAGES: Our examination revealed, for the first time, that MFNG exhibited high expression levels during EndMT of heart valve development in mice. Our findings provide compelling evidence that MFNG plays a role in promoting EndMT mediated by the Notch signalling pathway. Our results identified, for the first time, a deleterious MFNG p. T77M variant that inhibited the EndMT process by downregulating the activity of the Notch signalling pathway, thereby preventing the normal valve formation. MFNG may serve as an early diagnostic marker and an effective therapeutic target for the clinical treatment of congenital heart valve defects.

01 Jan 2025·Gene

Immune-related glycosylation genes based classification predicts prognosis and therapy options of osteosarcoma

Article

Author: Wang, Wen ; Jiao, Yunjia ; Du, Xiaojing ; Ye, Zhaoming

Osteosarcoma is the most common primary bone malignancy, with a very poor prognosis. Aberrant glycosylation is close involvement in osteosarcoma. Accordingly, this study aimed at investigating the role of glycosylation genes in the prognosis and therapy options of osteosarcoma. The microenvironment of osteosarcoma was assessed using estimate algorithm. A total of 20 immune-related glycosylation genes (IRGGs) was identified using Pearson correlation analysis. Accordingly, osteosarcoma patients were divided into C1 and C2 type using consensus clustering. Multiple algorithms (Xcell, MCP-counter, ssGSEA, epic, quantiseq), cancer immune cycle analysis, and GSVA were applied to estimate the immune, molecule and metabolism characteristics of osteosarcoma, indicating that C1 type was featured with high immune infiltration, high glycosylation, enriched MEK signaling, and good prognosis, while C2 type was characterized by more metastasis, enriched immunotherapy-positive gene signatures, high tumor mutation burden, and poor prognosis. Results from TIDE algorithm and immunotherapy datasets suggested the C2 type's preference of immune checkpoint inhibitors (ICIs), while data of GDSC, CMap analysis and cell experiments indicated that C1 type was sensitivity to MEK inhibitor PD0325901. In addition, univariate Cox and Lasso analysis was combined to establish an IRGGs' risk score containing 6 genes (B3GNT8, FUT7, GAL3ST4, GALNT14, HS3ST2, and MFNG). The data of DCA and ROC indicated its well prediction of prognosis in osteosarcoma. Finally, cellular location analysis showed that the 6 genes not only distributed in tumor cells but also in immune cells. In summary, the classification and risk score based on IRGGs effectively predicted the prognosis and therapy options of osteosarcoma. Further studies on IRGGs may contribute to the understanding of cancer immunity in osteosarcoma.

01 Jan 2024·The Journal of Gene Medicine

Artificial neural network‐based gene screening and immune cell infiltration analysis of osteosarcoma feature

Article

Author: Guo, Yunshan ; Huang, Yansheng ; Wang, Qian ; Shi, Shaoyan

AbstractBackgroundThe present study aimed to construct an artificial neural network (ANN) model that leverages characteristic genes associated with osteosarcoma (OS) to enable accurate prognostication for OS patients.MethodsOur research revealed 467 differentially expressed genes (DEGs) via gene expression contrast analysis, consisting of 345 downregulated genes and 122 upregulated genes. Gene Ontology (GO) enrichment analysis illuminated functions primarily encompassing T‐cell activation, secretory granule lumen and antioxidant activity, among others. Through Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, we discovered significant correlations between the DEGs and certain pathways, including phagosome, Staphylococcus aureus infection and human T‐cell leukemia virus 1 infection. We then screened out 30 characteristic DEGs (CDEGs) based on random forest analysis and constructed the ANN model using the gene score matrix. To verify the credibility and accuracy of the ANN model, we performed internal and external validation processes, which affirmed our model's predictive capabilities.ResultsThe study further delved into the analysis of immune cell infiltration and its correlation with the target CDEGs, revealing disparities in the infiltration of 22 types of immune cells across different groups and their interrelationships. Moreover, we probed the expression of the two foremost CDEGs (YES1 and MFNG) in OS and normal tissues. We noted a positive relationship between the expression of YES1 and MFNG in OS tissues and the clinicopathological characteristics of OS patients.ConclusionsCollectively, the findings of the present study validate the effectiveness of the CDEGs‐based ANN model in predicting OS patients, which might facilitate early diagnosis and treatment of OS.

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