Agarwal, S. Molecular pathology of the MEN1 gene. NY Acad. Hughes, C. Menin associates with a trithorax family histone methyltransferase complex and with the hoxc8 locus. Cell 13 , — Shilatifard, A. Molecular implementation and physiological roles for histone H3 lysine 4 H3K4 methylation. Cell Biol. Bernstein, B. Methylation of histone H3 Lys 4 in coding regions of active genes. USA 99 , — Noma, K.
Transitions in distinct histone H3 methylation patterns at the heterochromatin domain boundaries. Histone H3 lysine 4 methylation is mediated by Set1 and promotes maintenance of active chromatin states in fission yeast. USA 99 , Suppl 4 : — Santos-Rosa, H. Active genes are tri-methylated at K4 of histone H3. Scacheri, P. Genome-wide analysis of menin binding provides insights into MEN1 tumorigenesis. PLoS Genet. Li, B. Distinct pathways regulated by menin and by MLL1 in hematopoietic stem cells and developing B cells.
Blood , — Bres, V. Cell 36 , 75—87 Conacci-Sorrell, M. An overview of MYC and its interactome. Distribution of Menin-occupied regions in chromatin specifies a broad role of Menin in transcriptional regulation. Neoplasia 9 , — Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors. Vermeulen, M. Grasping trimethylation of histone H3 at lysine 4. Epigenomics 2 , — Li, Y. Structural basis for activity regulation of MLL family methyltransferases.
Gao, S. Suppression of lung adenocarcinoma through menin and polycomb gene-mediated repression of growth factor pleiotrophin.
Oncogene 28 , — Kim, H. Menin, a tumor suppressor, represses JunD-mediated transcriptional activity by association with an mSin3A-histone deacetylase complex. Cancer Res. Blackwood, E. Max: a helix-loop-helix zipper protein that forms a sequence-specific DNA-binding complex with Myc.
Karnik, S. Menin regulates pancreatic islet growth by promoting histone methylation and expression of genes encoding p27Kip1 and p18INK4c. Milne, T. Menin and MLL cooperatively regulate expression of cyclin-dependent kinase inhibitors. Bouchard, C. My1c-induced proliferation and transformation require Akt-mediated phosphorylation of FoxO proteins. EMBO J. Eberhardy, S. Kanazawa, S. Oncogene 22 , — Myc recruits P-TEFb to mediate the final step in the transcriptional activation of the cad promoter.
Huang, J. Zhou, Q. RNA polymerase II elongation control. Chao, S.
- C-Myc Function in Neoplasia : C V Dang : .
- Integrity: The Courage to Meet the Demands of Reality.
- MYC Activation Is a Hallmark of Cancer Initiation and Maintenance.
Igal, R. Stearoyl-CoA desaturase a novel key player in the mechanisms of cell proliferation, programmed cell death and transformation to cancer. Carcinogenesis 31 , — Shi, X. Regulation of lipid droplet size and phospholipid composition by stearoyl-CoA desaturase. Lipid Res. Scaglia, N. Stearoyl-CoA desaturase is involved in the control of proliferation, anchorage-independent growth, and survival in human transformed cells. Alderton, G.
Transcription: the transcriptional effects of MYC. Cancer 14 , — Cunningham, J.
c-Myc Function in Neoplasia - Chi V Dang, Linda A Lee - Häftad () | Bokus
Protein and nucleotide biosynthesis are coupled by a single rate-limiting enzyme, PRPS2, to drive cancer. Tseng, Y. Nature , 82—86 Carroll, P. Cancer Cell 27 , — Thomas, L. Cell 58 , — Ullius, A. Nucleic acids Res. MYC and transcription elongation.
Menin enhances c-Myc-mediated transcription to promote cancer progression
Gene regulation: fine-tuned amplification in cells. Zhang, H. Cancer Cell 11 , — Schnepp, R. Menin induces apoptosis in murine embryonic fibroblasts. Hermeking, H. USA 97 , — Download references.
We are grateful to Drs Chi V. All the authors read and approved the manuscript. Correspondence to Huafeng Zhang or Ping Gao. This work is licensed under a Creative Commons Attribution 4.
National Comprehensive Cancer Network
Reprints and Permissions. Endocrinology Human Molecular Genetics Molecular Therapy - Nucleic Acids Cancer Letters Cancer By submitting a comment you agree to abide by our Terms and Community Guidelines.
If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate. Advanced search. As a result of synergistic or sequential damage of DNA in normal colonic epithelial cells, several proto-oncogenes, including c-MYC are activated in parallel with the inactivation of tumor suppressor genes, leading finally to the alteration of DNA repair systems and apoptosis regulation. Accumulation of the damaged DNA may ultimately cause cellular transformation.