ArticleMolecular therapy. Nucleic acids2019
Menin Coordinates C/EBPβ-Mediated TGF-β Signaling for Epithelial-Mesenchymal Transition and Growth Inhibition in Pancreatic Cancer.
Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- Pancreatic cancer EMT‑targeted therapy: Molecular mechanisms and clinical translation (Review).International journal of oncology · 2026Review
- CEBPB emerges as a key regulatory factor in human cancers through diverse molecular mechanisms and clinical implications.Discover oncology · 2025Review
- Menin facilitates the cell proliferation of bladder cancer via modulating the TFAP2C/β-catenin axis.Genes & diseases · 2025Article
- A CEBPB/TYMP/GDF15 signaling axis mediates tumor growth and cisplatin resistance in bladder cancer.Translational oncology · 2025Article
- Menin regulates YBX1 nucleus translocation to boost the HKDC1 transcription and affects pancreatic cancer glycolysis.iScience · 2025Article
- Familial MEN1 Syndrome with Atypical Renal Features and a Coexisting CLDN16 Variant: A Case Series.Journal of clinical medicine · 2025Article
- Phytochemical profiling and anticancer potential of pistachio wastes against MCF-7 breast cancer cells: a metabolic and apoptotic pathway analysis.BMC complementary medicine and therapies · 2025Article
- CEBPB promotes transformation of endometrial complex atypical hyperplasia to endometrial cancer.BMC cancer · 2025Article
- LncRNA MIR503HG regulates NETs-mediated NLRP3 inflammasome activation and NSCLC metastasis by enhancing the ubiquitination of C/EBPβ.Clinical and translational medicine · 2025Article
- Menin: from molecular insights to clinical impact.Epigenomics · 2025Review
- Investigating synthetic lethality and PARP inhibitor resistance in pancreatic cancer through enantiomer differential activity.Cell death discovery · 2025Article
- DNA methylation biomarker analysis from low-survival-rate cancers based on genetic functional approaches.Frontiers in bioinformatics · 2025Article
- Menin in Cancer.Genes · 2024Review
- Noninvasive assessment of organ-specific and shared pathways in multi-organ fibrosis using T1 mapping.Nature medicine · 2024Article
- Prioritization of risk genes in colorectal cancer by integrative analysis of multi-omics data and gene networks.Science China. Life sciences · 2024Article
- Epigenetic control of pancreatic cancer metastasis.Cancer metastasis reviews · 2023Review
- Chromatin accessibility uncovers KRAS-driven FOSL2 promoting pancreatic ductal adenocarcinoma progression through up-regulation of CCL28.British journal of cancer · 2023Article
- Article
- C/EBP-Family Redundancy Determines Patient Survival and Lymph Node Involvement in PDAC.International journal of molecular sciences · 2023Article
- Evaluating the role of MEN1 gene expression and its clinical significance in breast cancer patients.PloS one · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Menin displays either tumor suppression or promotion functions in a context-dependent manner. Previously, we proposed that Menin acts as a tumor suppressor by inhibiting cell growth in pancreatic ductal adenocarcinoma (PDAC), whereas the relationship between the Menin expression and overall survival rate of PDAC patients has not been completely elucidated, indicating the complexity of Menin functions in PDAC progression. Here, we identify Menin as a promoter of epithelial-mesenchymal transition (EMT), which is largely associated with cell migration or metastasis, with modest activity in cell growth inhibition. Ectopic expression of Menin suppresses the expression of CCAAT/enhancer-binding protein beta (CEBPB) and epithelial-specific genes by histone deacetylation and further enhances the TGF-β signaling-related EMT process. We also demonstrate that CCAAT/enhancer binding protein (C/EBP) beta (C/EBPβ; encoded by CEBPB) acts downstream of Menin and TGF-β signaling for balancing growth inhibition and EMT, and C/EBPβ overexpression could restore the anti-cancer functions of Menin in pancreatic cancer by cooperatively activating CDKN2A/B genes and antagonizing EMT processes. Taken together, our results suggest that Menin functions as an oncogene for cancer metastasis upon C/EBPβ depletion or acts as a tumor suppressor by cooperation with C/EBPβ to activate CDKN2A transcription.
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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.