Document Detail


Menin, histone h3 methyltransferases, and regulation of cell proliferation: current knowledge and perspective.
MedLine Citation:
PMID:  19075677     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Menin is a tumor suppressor encoded by the MEN1 gene that is mutated in patients with an inherited syndrome, multiple endocrine neoplasia type 1 (MEN1). Loss of menin has potent impact on proliferation of endocrine and non-endocrine cells. However, until recently little has been known as to how menin regulates cell proliferation. Rapid research progress in the past several years suggests that menin represses proliferation of endocrine cells yet promotes proliferation in certain types of leukemia cells via interacting with various transcriptional regulators. Menin interacts with histone H3 methyltransferases such as MLL (mixed lineage leukemia) protein. Increasing evidence has linked the biological function of menin to epigenetic histone modifications, control of the pattern of gene expression, and regulation of cell proliferation in a cell type-specific manner. In light of these recent findings, an emerging model suggests that menin is a crucial regulator of histone modifiers by acting as a scaffold protein to coordinate gene transcription and cell proliferation in a cell context-dependent manner. This recent progress unravels the coordinating role of menin in epigenetics and regulation of cell cycle, providing novel insights into understanding regulation of beta cell functions and diabetes, as well as the development and therapy of endocrine tumors and leukemia.
Authors:
Xinjiang Wu; Xianxin Hua
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Current molecular medicine     Volume:  8     ISSN:  1566-5240     ISO Abbreviation:  Curr. Mol. Med.     Publication Date:  2008 Dec 
Date Detail:
Created Date:  2008-12-16     Completed Date:  2009-02-04     Revised Date:  2013-07-12    
Medline Journal Info:
Nlm Unique ID:  101093076     Medline TA:  Curr Mol Med     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  805-15     Citation Subset:  IM    
Affiliation:
Abramson Family Cancer Research Institute, Department of Cancer Biology, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
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MeSH Terms
Descriptor/Qualifier:
Cell Proliferation*
Genes, Tumor Suppressor
Histone-Lysine N-Methyltransferase
Humans
Leukemia, Biphenotypic, Acute / genetics,  pathology,  physiopathology
Models, Biological
Multiple Endocrine Neoplasia Type 1 / genetics,  pathology,  physiopathology
Myeloid-Lymphoid Leukemia Protein / genetics,  physiology
Protein Methyltransferases / physiology*
Proto-Oncogene Proteins / genetics,  physiology*
Translocation, Genetic
Grant Support
ID/Acronym/Agency:
R01 CA100912/CA/NCI NIH HHS; R01 CA100912/CA/NCI NIH HHS; R01 CA100912-03/CA/NCI NIH HHS; R01 CA100912-04/CA/NCI NIH HHS; R01 CA113962/CA/NCI NIH HHS; R01 CA113962/CA/NCI NIH HHS; R01 CA113962-02/CA/NCI NIH HHS; R01 CA113962-03/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/MEN1 protein, human; 0/Proto-Oncogene Proteins; 149025-06-9/Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.-/Protein Methyltransferases; EC 2.1.1.-/histone methyltransferase; EC 2.1.1.43/Histone-Lysine N-Methyltransferase
Comments/Corrections

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