ArticleCancer research2015
Manic fringe promotes a claudin-low breast cancer phenotype through notch-mediated PIK3CG induction.
Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Functional Gene Expression Differentiation of the Notch Signaling Pathway in Female Reproductive Tract Tissues-A Comprehensive Review With Analysis.Frontiers in cell and developmental biology · 2020Pooled it
- Notch receptors in breast cancer: context-dependent roles and therapeutic targeting.Cell communication and signaling : CCS · 2026Review
- Glycosylation-Related Gene Signature Identifies MFNG as a Key Driver of Proliferation and Metastasis in Colorectal Cancer.OncoTargets and therapy · 2026Article
- Down-regulation of MFNG promotes the metastatic potential of lung adenocarcinoma by regulating TGF-β/Smad signaling.iScience · 2025Article
- The involvement of exosomes in the tumorigenicity of breast cancer cell lines through the crosstalk between STAT3, Notch, and Wnt signaling pathways.Discover oncology · 2025Article
- Prognostic implication of endoplasmic reticulum stress-related gene signature in lung adenocarcinoma and its effect on tumor immunity.Translational cancer research · 2025Article
- Overexpression of PIK3CG in Cancer Cells Promotes Lung Cancer Cell Migration and Metastasis Through Enhanced MMPs Expression and Neutrophil Recruitment and Activation.Biochemical genetics · 2025Article
- Raman spectroscopy and bioinformatics-based identification of key genes and pathways capable of distinguishing between diffuse large B cell lymphoma and chronic lymphocytic leukemia.Frontiers in immunology · 2025Article
- MAPK Signaling-Mediated RFNG Phosphorylation and Nuclear Translocation Restrain Oxaliplatin-Induced Apoptosis and Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Prediction of immunotherapy response using mutations to cancer protein assemblies.Science advances · 2024Article
- Beauvericin Reverses Epithelial-to-Mesenchymal Transition in Triple-Negative Breast Cancer Cells through Regulation of Notch Signaling and Autophagy.ACS pharmacology & translational science · 2024Article
- Tumor suppressor FRMD3 controls mammary epithelial cell fate determination via notch signaling pathway.Science advances · 2024Article
- Notch signaling pathway in cancer: from mechanistic insights to targeted therapies.Signal transduction and targeted therapy · 2024Review
- Therapeutic potential of anti-PIK3CG treatment for multiple myeloma via inhibiting c-Myc pathway.Heliyon · 2024Article
- Distinct mRNA expression profiles and miRNA regulators of the PI3K/AKT/mTOR pathway in breast cancer: insights into tumor progression and therapeutic targets.Frontiers in oncology · 2024Article
- Prognostic determinants and functional role of PIK3C2G in stage IIb-IIIa lung adenocarcinoma: insights from clinical and molecular analyses.Frontiers in oncology · 2024Article
- A pan-cancer analysis revealing the role of LFNG, MFNG and RFNG in tumor prognosis and microenvironment.BMC cancer · 2023Article
- MFNG is an independent prognostic marker for osteosarcoma.European journal of medical research · 2023Article
- New Biomarkers and Treatment Advances in Triple-Negative Breast Cancer.Diagnostics (Basel, Switzerland) · 2023Review
- Molecular basis for differential activation of p101 and p84 complexes of PI3Kγ by Ras and GPCRs.Cell reports · 2023Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 3 countries.
Funding
Abstract
Claudin-low breast cancer (CLBC) is a poor prognosis disease biologically characterized by stemness and mesenchymal features. These tumors disproportionately affect younger patients and women with African ancestry, causing significant morbidity and mortality, and no effective targeted therapy exists at present. CLBC is thought to originate from mammary stem cells, but little is known on how or why these tumors express a stable epithelial-to-mesenchymal transition phenotype, or what are the driving forces of this disease. Here, we report that Manic Fringe (Mfng), which encodes an O-fucosylpeptide 3-β-N-acetylglucosaminyltransferase known to modify EGF repeats in the Notch extracellular domain, is highly expressed in CLBC and functions as an oncogene in this context. We show that Mfng modulates Notch activation in human and mouse CLBC cell lines, as well as in mouse mammary gland. Mfng silencing in CLBC cell lines reduced cell migration, tumorsphere formation, and in vivo tumorigenicity associated with a decrease in the stem-like cell population. Mfng deletion in the Lfng(flox/flox);MMTV-Cre mouse model, in which one-third of mammary tumors resemble human CLBC, caused a tumor subtype shift away from CLBC. We identified the phosphoinositide kinase Pik3cg as a direct transcriptional target of Mfng-facilitated RBPJκ-dependent Notch signaling. Indeed, pharmacologic inhibition of PI3Kγ in CLBC cell lines blocked migration and tumorsphere formation. Taken together, our results define Mfng as an oncogene acting through Notch-mediated induction of Pik3cg. Furthermore, they suggest that targeting PI3Kγ may prove beneficial for the treatment of CLBC subtype.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.