ArticleMolecular cancer research : MCR2013
Menin directly represses Gli1 expression independent of canonical Hedgehog signaling.
Article in Molecular cancer research : MCR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Hedgehog signaling drives glial cell plasticity and oncogenic reprogramming in gastroenteropancreatic neuroendocrine neoplasms.Molecular cancer · 2026Article
- The regulation roles of miRNAs in Helicobacter pylori infection.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Research progress on PRMTs involved in epigenetic modification and tumour signalling pathway regulation (Review).International journal of oncology · 2023Review
- Multiprotein GLI Transcriptional Complexes as Therapeutic Targets in Cancer.Life (Basel, Switzerland) · 2022Review
- Chitosan nanoparticle-mediated effect of antimiRNA-324-5p on decreasing the ovarian cancer cell proliferation by regulation of GLI1 expression.BioImpacts : BI · 2022Article
- A novel mechanism of regulation of the oncogenic transcription factor GLI3 by toll-like receptor signaling.Oncotarget · 2022Article
- Epigenetic Regulation in Gastroenteropancreatic Neuroendocrine Tumors.Frontiers in oncology · 2022Review
- The Effects of Hedgehog Signaling Pathway on the Proliferation and Apoptosis of Melanoma Cells.Journal of oncology · 2022Article
- A Blood-based Polyamine Signature Associated With MEN1 Duodenopancreatic Neuroendocrine Tumor Progression.The Journal of clinical endocrinology and metabolism · 2021Article
- The uncharacterized protein FAM47E interacts with PRMT5 and regulates its functions.Life science alliance · 2021Article
- Circ-GLI1 promotes metastasis in melanoma through interacting with p70S6K2 to activate Hedgehog/GLI1 and Wnt/β-catenin pathways and upregulate Cyr61.Cell death & disease · 2020Article
- PRMT5 function and targeting in cancer.Cell stress · 2020Review
- Non-canonical Hedgehog Signaling Pathway in Cancer: Activation of GLI Transcription Factors Beyond Smoothened.Frontiers in genetics · 2019Review
- MENIN loss as a tissue-specific driver of tumorigenesis.Molecular and cellular endocrinology · 2018Review
- Targeted therapy of gastroenteropancreatic neuroendocrine tumours: preclinical strategies and future targets.Endocrine connections · 2018Review
- Twenty years of menin: emerging opportunities for restoration of transcriptional regulation in MEN1.Endocrine-related cancer · 2017Review
- The future: genetics advances in MEN1 therapeutic approaches and management strategies.Endocrine-related cancer · 2017Review
- Epigenetic regulation by the menin pathway.Endocrine-related cancer · 2017Review
- Menin and PRMT5 suppress GLP1 receptor transcript and PKA-mediated phosphorylation of FOXO1 and CREB.American journal of physiology. Endocrinology and metabolism · 2017Article
- Role of Sonic Hedgehog Signaling in Oligodendrocyte Differentiation.Neurochemical research · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
unlabelledMultiple endocrine neoplasia type 1 (MEN-1), is a familial tumor syndrome resulting from mutations in the tumor suppressor gene menin (MEN1). Menin plays an essential role in both repressing and activating gene expression. However, it is not well understood how menin represses expression of multiple genes. Upon MEN1 excision, the transcription factor Gli1 and its target genes, including Ptch1 and c-Myc, were shown to be elevated in the absence of an apparent Hedgehog) pathway-activating ligand or when Smoothened (SMO), a key component of the pathway, is inhibited. Menin binds to the GLI1 promoter and recruits PRMT5, a histone arginine methyltransferase associated with transcriptional repression. Both PRMT5 binding and histone H4 arginine 3 methylation (H4R3m2s) are decreased at the GLI1 promoter in MEN1-excised cells. Moreover, MEN1 ablation resulted in increased binding of transcriptionally active Gli1 at the GLI1 promoter in a manner not influenced by the canonical Hedgehog signaling pathway. Inhibition of Gli1 by the small-molecule inhibitor GANT-61 led to decreased expression of Gli1 and its target genes in MEN1-depeleted cells. Furthermore, GANT-61 potently suppressed proliferation of MEN1-excised cells as compared with control cells. These findings uncover a novel epigenetic link whereby menin directly represses Gli1 expression, independent of the canonical Hedgehog signaling pathway, via PRMT5 and its repressive H4R3m2s mark. IMPLICATIONS: Inhibition of GLI1 suppresses neuroendocrine tumors harboring mutations in the MEN1 gene.
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