ArticleEndocrine-related cancer2013
The embryonic transcription factor Hlxb9 is a menin interacting partner that controls pancreatic β-cell proliferation and the expression of insulin regulators.
Article in Endocrine-related cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- MEN1-Related Neuroendocrine Tumors Show c-MET Overexpression.Journal of the Endocrine Society · 2025Article
- Pancreatic Differentiation of Oral Minor Salivary Gland Stem Cells.Stem cell reviews and reports · 2024Article
- Effect of transcription factor MEOX on insulin gene expression in glucagon-like peptide 1-secreting cells.In vitro cellular & developmental biology. Animal · 2024Article
- Menin in Cancer.Genes · 2024Review
- Menin orchestrates hepatic glucose and fatty acid uptake via deploying the cellular translocation of SIRT1 and PPARγ.Cell & bioscience · 2023Article
- Molecular and Clinical Spectrum of Primary Hyperparathyroidism.Endocrine reviews · 2023Article
- Review
- Multiple Endocrine Neoplasia Type 1: Latest Insights.Endocrine reviews · 2021Review
- Article
- Wild-type menin is rapidly degraded via the ubiquitin-proteasome pathway in a rat insulinoma cell line.Bioscience reports · 2019Article
- Functional Defects From Endocrine Disease-Associated Mutations in HLXB9 and Its Interacting Partner, NONO.Endocrinology · 2018Article
- Menin Modulates Mammary Epithelial Cell Numbers in Bovine Mammary Glands Through Cyclin D1.Journal of mammary gland biology and neoplasia · 2017Article
- Long Noncoding RNA MEG3 Is an Epigenetic Determinant of Oncogenic Signaling in Functional Pancreatic Neuroendocrine Tumor Cells.Molecular and cellular biology · 2017Article
- The future: genetics advances in MEN1 therapeutic approaches and management strategies.Endocrine-related cancer · 2017Review
- Twenty years of menin: emerging opportunities for restoration of transcriptional regulation in MEN1.Endocrine-related cancer · 2017Review
- MEN1/Menin regulates milk protein synthesis through mTOR signaling in mammary epithelial cells.Scientific reports · 2017Article
- A Review of the Scaffold Protein Menin and its Role in Hepatobiliary Pathology.Gene expression · 2017Review
- Inactivating the permanent neonatal diabetes gene Mnx1 switches insulin-producing β-cells to a δ-like fate and reveals a facultative proliferative capacity in aged β-cells.Development (Cambridge, England) · 2015Article
- Pro-oncogenic Roles of HLXB9 Protein in Insulinoma Cells through Interaction with Nono Protein and Down-regulation of the c-Met Inhibitor Cblb (Casitas B-lineage Lymphoma b).The Journal of biological chemistry · 2015Article
- Epigenetic regulation of the lncRNA MEG3 and its target c-MET in pancreatic neuroendocrine tumors.Molecular endocrinology (Baltimore, Md.) · 2015Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
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Abstract
The multiple endocrine neoplasia type 1 (MEN1) syndrome is caused by germline mutations in the MEN1 gene encoding menin, with tissue-specific tumors of the parathyroids, anterior pituitary, and enteropancreatic endocrine tissues. Also, 30-40% of sporadic pancreatic endocrine tumors show somatic MEN1 gene inactivation. Although menin is expressed in all cell types of the pancreas, mouse models with loss of menin in either pancreatic α-cells, or β-cells, or total pancreas develop β-cell-specific endocrine tumors (insulinomas). Loss of widely expressed tumor suppressor genes may produce tissue-specific tumors by reactivating one or more embryonic-specific differentiation factors. Therefore, we determined the effect of menin overexpression or knockdown on the expression of β-cell differentiation factors in a mouse β-cell line (MIN6). We show that the β-cell differentiation factor Hlxb9 is posttranscriptionally upregulated upon menin knockdown, and it interacts with menin. Hlxb9 reduces cell proliferation and causes apoptosis in the presence of menin, and it regulates genes that modulate insulin level. Thus, upon menin loss or from other causes, dysregulation of Hlxb9 predicts a possible combined mechanism for β-cell proliferation and insulin production in insulinomas. These observations help to understand how a ubiquitously expressed protein such as menin might control tissue-specific tumorigenesis. Also, our findings identify Hlxb9 as an important factor for β-cell proliferation and insulin regulation.
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Registered trials
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