ArticleMolecular and cellular biology2013
MEN1 is a melanoma tumor suppressor that preserves genomic integrity by stimulating transcription of genes that promote homologous recombination-directed DNA repair.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
- Ocular morbidity in uveal melanocytoma associated with MEN1 syndrome.American journal of ophthalmology case reports · 2026Article
- The tumor suppressor menin is a key scaffold mediator for homologous recombination repair.Nucleic acids research · 2026Article
- Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Alpha-synuclein knockout impairs melanoma development and alters DNA damage repair in the TG3 mouse model in a sex-dependent manner.Frontiers in oncology · 2025Article
- Molecular Basis of Pancreatic Neuroendocrine Tumors.International journal of molecular sciences · 2024Review
- Menin in Cancer.Genes · 2024Review
- Loss of tumor suppressor menin expression in high grade cholangiocarcinomas.BMC research notes · 2023Article
- Cutaneous lesions and other non-endocrine manifestations of Multiple Endocrine Neoplasia type 1 syndrome.Frontiers in endocrinology · 2023Article
- Loss of TDP-43 function contributes to genomic instability in amyotrophic lateral sclerosis.Frontiers in neuroscience · 2023Article
- Identification of DNA repair gene signature and potential molecular subtypes in hepatocellular carcinoma.Frontiers in oncology · 2023Article
- Approach of Multiple Endocrine Neoplasia Type 1 (MEN1) Syndrome-Related Skin Tumors.Diagnostics (Basel, Switzerland) · 2022Review
- Loss of MEN1 function impairs DNA repair capability of pancreatic neuroendocrine tumors.Endocrine-related cancer · 2022Article
- Beyond the "3 Ps": A critical appraisal of the non-endocrine manifestations of multiple endocrine neoplasia type 1.Frontiers in endocrinology · 2022Review
- Article
- Mutational landscape and potential therapeutic targets for sporadic pancreatic neuroendocrine tumors based on target next-generation sequencing.Experimental and therapeutic medicine · 2021Article
- Clinical aspects of multiple endocrine neoplasia type 1.Nature reviews. Endocrinology · 2021Review
- ARMC5 Alterations in Patients With Sporadic Neuroendocrine Tumors and Multiple Endocrine Neoplasia Type 1 (MEN1).The Journal of clinical endocrinology and metabolism · 2020Article
- Development and validation of a DNA repair gene signature for prognosis prediction in Colon Cancer.Journal of Cancer · 2020Article
- Biomarkers for Pancreatic Neuroendocrine Neoplasms (PanNENs) Management-An Updated Review.Frontiers in oncology · 2020Review
- Genetics and Epigenetics of Gastroenteropancreatic Neuroendocrine Neoplasms.Endocrine reviews · 2019Review
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
Abstract
Multiple endocrine neoplasia type 1 is a familial cancer syndrome resulting from loss-of-function mutations in the MEN1 gene. We previously identified the tumor suppressor MEN1 as a gene required for oncogene-induced senescence in melanocytes, raising the possibility that MEN1 is a melanoma tumor suppressor. Here we show that MEN1 expression is lost in a high percentage of human melanomas and melanoma cell lines. We find that melanocytes depleted of MEN1 are deficient in homologous recombination (HR)-directed DNA repair, which is accompanied by increased nonhomologous end-joining activity. Following DNA damage, MEN1 levels increase as a result of phosphorylation by the DNA damage kinase ATM/ATR. Most importantly, we show that MEN1 functions by directly stimulating the transcription of several genes, including BRCA1, RAD51, and RAD51AP1, that encode proteins involved in HR. MEN1 and its coactivator, the mixed-lineage leukemia histone methyltransferase, are recruited to the BRCA1, RAD51, and RAD51AP1 promoters by estrogen receptor 1, resulting in increased histone H3-lysine 4 trimethylation and transcription. Collectively, our results indicate that MEN1 is a melanoma tumor suppressor that functions by stimulating the transcription of genes involved in HR-directed DNA repair.
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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.