c-Myc

Summary

Gene Symbol: c-Myc
Description: MYC proto-oncogene, bHLH transcription factor
Alias: MRTL, MYCC, bHLHe39, c-Myc, myc proto-oncogene protein, avian myelocytomatosis viral oncogene homolog, class E basic helix-loop-helix protein 39, myc-related translation/localization regulatory factor, proto-oncogene c-Myc, transcription factor p64, v-myc avian myelocytomatosis viral oncogene homolog, v-myc myelocytomatosis viral oncogene homolog
Species: human
Products:     c-Myc

Top Publications

  1. Porro A, Iraci N, Soverini S, Diolaiti D, Gherardi S, Terragna C, et al. c-MYC oncoprotein dictates transcriptional profiles of ATP-binding cassette transporter genes in chronic myelogenous leukemia CD34+ hematopoietic progenitor cells. Mol Cancer Res. 2011;9:1054-66 pubmed publisher
  2. Johnson N, Slack G, Savage K, Connors J, Ben Neriah S, Rogic S, et al. Concurrent expression of MYC and BCL2 in diffuse large B-cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone. J Clin Oncol. 2012;30:3452-9 pubmed
    ..Assessment of MYC and BCL2 expression by IHC represents a robust, rapid, and inexpensive approach to risk-stratify patients with DLBCL at diagnosis. ..
  3. Cho Y, Tsherniak A, Tamayo P, Santagata S, Ligon A, Greulich H, et al. Integrative genomic analysis of medulloblastoma identifies a molecular subgroup that drives poor clinical outcome. J Clin Oncol. 2011;29:1424-30 pubmed publisher
    ..Our results detail the complex genomic heterogeneity of medulloblastomas and identify a previously unrecognized molecular subgroup with poor clinical outcome for which more effective therapeutic strategies should be developed. ..
  4. Goode E, Chenevix Trench G, Song H, Ramus S, Notaridou M, Lawrenson K, et al. A genome-wide association study identifies susceptibility loci for ovarian cancer at 2q31 and 8q24. Nat Genet. 2010;42:874-9 pubmed publisher
    ..Analysis of HOXD1, MYC, TIPARP and SKAP1 at these loci and of BNC2 at 9p22 supports a functional role for these genes in ovarian cancer development. ..
  5. Darcy K, Brady W, Blancato J, Dickson R, Hoskins W, McGuire W, et al. Prognostic relevance of c-MYC gene amplification and polysomy for chromosome 8 in suboptimally-resected, advanced stage epithelial ovarian cancers: a Gynecologic Oncology Group study. Gynecol Oncol. 2009;114:472-9 pubmed publisher
    ..c-MYC amplification and polysomy 8 have limited predictive or prognostic value in suboptimally-resected, advanced stage EOC treated with platinum-based combination chemotherapy. ..
  6. Prensner J, Chen W, Han S, Iyer M, Cao Q, Kothari V, et al. The long non-coding RNA PCAT-1 promotes prostate cancer cell proliferation through cMyc. Neoplasia. 2014;16:900-8 pubmed publisher
    ..This work establishes a basis for the oncogenic role of PCAT-1 in cancer cell proliferation and is the first study to implicate lncRNAs in the regulation of cMyc in prostate cancer. ..
  7. Chan S, Weng A, Tibshirani R, Aster J, Utz P. Notch signals positively regulate activity of the mTOR pathway in T-cell acute lymphoblastic leukemia. Blood. 2007;110:278-86 pubmed
    ..T-ALL cell growth was suppressed in a highly synergistic manner by simultaneous treatment with the mTOR inhibitor rapamycin and GSI, which represents a rational drug combination for treating this aggressive human malignancy. ..
  8. Gonzalez V, Guo K, Hurley L, Sun D. Identification and characterization of nucleolin as a c-myc G-quadruplex-binding protein. J Biol Chem. 2009;284:23622-35 pubmed publisher
    ..Finally, we show that nucleolin binds to the c-myc promoter in HeLa cells, which indicates that this interaction occurs in vivo. In summary, nucleolin may induce c-myc G4 formation in vivo. ..
  9. Wright J, Brown S, Cole M. Upregulation of c-MYC in cis through a large chromatin loop linked to a cancer risk-associated single-nucleotide polymorphism in colorectal cancer cells. Mol Cell Biol. 2010;30:1411-20 pubmed publisher
    ..The findings of these studies support a mechanism for intergenic SNPs that can promote cancer through the regulation of distal genes by utilizing preexisting large chromatin loops. ..

More Information

Publications180 found, 100 shown here

  1. Nikiforov M, Chandriani S, Park J, Kotenko I, Matheos D, Johnsson A, et al. TRRAP-dependent and TRRAP-independent transcriptional activation by Myc family oncoproteins. Mol Cell Biol. 2002;22:5054-63 pubmed
    ..Nevertheless, L-Myc is a potent activator of several basally expressed genes and can fully restore the growth defect of myc-null cells. These results suggest a differential requirement for TRRAP for several Myc-mediated activities. ..
  2. Vervoorts J, Lüscher Firzlaff J, Rottmann S, Lilischkis R, Walsemann G, Dohmann K, et al. Stimulation of c-MYC transcriptional activity and acetylation by recruitment of the cofactor CBP. EMBO Rep. 2003;4:484-90 pubmed
    ..Functionally, this results in a decrease in ubiquitination and stabilization of c-MYC proteins. Thus, CBP and p300 are novel functional binding partners of c-MYC. ..
  3. Hagio Y, Kimura Y, Taira T, Fujioka Y, Iguchi Ariga S, Ariga H. Distinct localizations and repression activities of MM-1 isoforms toward c-Myc. J Cell Biochem. 2006;97:145-55 pubmed
    ..These results suggest that each MM-1 isoform distinctly regulates c-Myc transcription activity in respective tissues. ..
  4. Ooi A, Suzuki S, Nakazawa K, Itakura J, Imoto I, Nakamura H, et al. Gene amplification of Myc and its coamplification with ERBB2 and EGFR in gallbladder adenocarcinoma. Anticancer Res. 2009;29:19-26 pubmed
    ..A case of polysomy 8 also demonstrated amplification of ERBB2 and EGFR. The present study shows that genomic instability due to Myc amplification may cause specific amplification of EGFR and/or ERBB2. ..
  5. Beharry Z, Mahajan S, Zemskova M, Lin Y, Tholanikunnel B, Xia Z, et al. The Pim protein kinases regulate energy metabolism and cell growth. Proc Natl Acad Sci U S A. 2011;108:528-33 pubmed publisher
    ..These results demonstrate the Pim kinase-mediated control of energy metabolism and thus regulation of AMPK activity. We identify an important role for Pim-3 in modulating c-Myc and PGC-1? protein levels and cell growth. ..
  6. Liu H, Radisky D, Yang D, Xu R, Radisky E, Bissell M, et al. MYC suppresses cancer metastasis by direct transcriptional silencing of ?v and ?3 integrin subunits. Nat Cell Biol. 2012;14:567-74 pubmed publisher
  7. Qi Y, Gregory M, Li Z, Brousal J, West K, Hann S. p19ARF directly and differentially controls the functions of c-Myc independently of p53. Nature. 2004;431:712-7 pubmed
    ..This direct feedback mechanism represents a p53-independent checkpoint to prevent c-Myc-mediated tumorigenesis. ..
  8. Smith D, Bath M, Metcalf D, Harris A, Cory S. MYC levels govern hematopoietic tumor type and latency in transgenic mice. Blood. 2006;108:653-61 pubmed
    ..The implication is that MYC level affects the spontaneous acquisition of synergistic oncogenic mutations. ..
  9. Cannell I, Kong Y, Johnston S, Chen M, Collins H, Dobbyn H, et al. p38 MAPK/MK2-mediated induction of miR-34c following DNA damage prevents Myc-dependent DNA replication. Proc Natl Acad Sci U S A. 2010;107:5375-80 pubmed publisher
  10. Matsushita K, Takenouchi T, Shimada H, Tomonaga T, Hayashi H, Shioya A, et al. Strong HLA-DR antigen expression on cancer cells relates to better prognosis of colorectal cancer patients: Possible involvement of c-myc suppression by interferon-gamma in situ. Cancer Sci. 2006;97:57-63 pubmed
  11. Chang T, Yu D, Lee Y, Wentzel E, Arking D, West K, et al. Widespread microRNA repression by Myc contributes to tumorigenesis. Nat Genet. 2008;40:43-50 pubmed
    ..We further show that enforced expression of repressed miRNAs diminishes the tumorigenic potential of lymphoma cells. These results demonstrate that extensive reprogramming of the miRNA transcriptome by Myc contributes to tumorigenesis. ..
  12. Lin S, Elledge S. Multiple tumor suppressor pathways negatively regulate telomerase. Cell. 2003;113:881-9 pubmed
    ..These studies suggest that multiple tumor suppressor/oncogene pathways coordinately repress hTERT expression and imply that telomerase is reactivated in human tumors through oncogenic mutations. ..
  13. Koshiji M, Kageyama Y, Pete E, Horikawa I, Barrett J, Huang L. HIF-1alpha induces cell cycle arrest by functionally counteracting Myc. EMBO J. 2004;23:1949-56 pubmed
    ..Hence, we propose that Myc is an integral part of a novel HIF-1alpha pathway, which regulates a distinct group of Myc target genes in response to hypoxia. ..
  14. Mu Z, Yin X, Prochownik E. Pag, a putative tumor suppressor, interacts with the Myc Box II domain of c-Myc and selectively alters its biological function and target gene expression. J Biol Chem. 2002;277:43175-84 pubmed
    ..These features, along with the previously identified interaction with c-Abl, provide support for the idea that Pag functions as a tumor suppressor. ..
  15. Liu X, Tesfai J, Evrard Y, Dent S, Martinez E. c-Myc transformation domain recruits the human STAGA complex and requires TRRAP and GCN5 acetylase activity for transcription activation. J Biol Chem. 2003;278:20405-12 pubmed
    ..Thus, TRRAP might function as an adaptor within the STAGA complex, which helps recruit GCN5 HAT activity to Myc during transcription activation. ..
  16. Datta A, Nag A, Pan W, Hay N, Gartel A, Colamonici O, et al. Myc-ARF (alternate reading frame) interaction inhibits the functions of Myc. J Biol Chem. 2004;279:36698-707 pubmed
    ..Our results strongly suggest that cMyc is a bona fide target of ARF and that ARF attenuates c-Myc independently of the ARF-p53 axis. ..
  17. Acosta J, Ferrandiz N, Bretones G, Torrano V, Blanco R, Richard C, et al. Myc inhibits p27-induced erythroid differentiation of leukemia cells by repressing erythroid master genes without reversing p27-mediated cell cycle arrest. Mol Cell Biol. 2008;28:7286-95 pubmed publisher
    ..Our results support the hypothesis that differentiation inhibition is an important Myc tumorigenic mechanism that is independent of cell proliferation. ..
  18. Li Y, Lu J, Prochownik E. Modularity of the oncoprotein-like properties of platelet glycoprotein Ibalpha. J Biol Chem. 2009;284:1410-8 pubmed publisher
    ..Together, these results provide strong evidence that the domains of GpIbalpha mediating c-Myc-like functions are modular, genetically distinct, and independent of those involved in vWFR signaling. ..
  19. Rottmann S, Wang Y, Nasoff M, Deveraux Q, Quon K. A TRAIL receptor-dependent synthetic lethal relationship between MYC activation and GSK3beta/FBW7 loss of function. Proc Natl Acad Sci U S A. 2005;102:15195-200 pubmed
    ..The results also demonstrate paradoxically that MYC-expressing tumors might be treatable by drug combinations that increase rather than decrease MYC oncoprotein function. ..
  20. Wu N, Rollin J, Masse I, Lamartine J, Gidrol X. p63 regulates human keratinocyte proliferation via MYC-regulated gene network and differentiation commitment through cell adhesion-related gene network. J Biol Chem. 2012;287:5627-38 pubmed publisher
    ..Furthermore, we show that the balance between the MYC-controlled cell cycle progression network and the p63-controlled cell adhesion-related network could dictate skin cell fate. ..
  21. Tuupanen S, Yan J, Turunen M, Gylfe A, Kaasinen E, Li L, et al. Characterization of the colorectal cancer-associated enhancer MYC-335 at 8q24: the role of rs67491583. Cancer Genet. 2012;205:25-33 pubmed publisher
  22. Zhang Q, Luo C, Wu X, Wang C, Xu X, Zhang Y, et al. HepaCAM induces G1 phase arrest and promotes c-Myc degradation in human renal cell carcinoma. J Cell Biochem. 2011;112:2910-9 pubmed publisher
    ..Thus, our research implies that the decrease in c-Myc protein expression, resulting from ectopic expression of hepaCAM, may contribute to the inhibition of proliferation in these cells. ..
  23. Schneider A, Peukert K, Eilers M, Hanel F. Association of Myc with the zinc-finger protein Miz-1 defines a novel pathway for gene regulation by Myc. Curr Top Microbiol Immunol. 1997;224:137-46 pubmed
    ..We have termed this protein Miz-1 (Myc-interacting zinc finger protein). Some of the properties of Miz-1 suggest that it may be involved in gene repression by Myc in vivo. ..
  24. Hoffman B, Amanullah A, Shafarenko M, Liebermann D. The proto-oncogene c-myc in hematopoietic development and leukemogenesis. Oncogene. 2002;21:3414-21 pubmed
    ..Understanding how c-Myc controls cellular phenotypes, including the leukemic phenotype, should provide novel tools for designing drugs to promote differentiation and/or apoptosis of leukemic cells. ..
  25. Jung P, Menssen A, Mayr D, Hermeking H. AP4 encodes a c-MYC-inducible repressor of p21. Proc Natl Acad Sci U S A. 2008;105:15046-51 pubmed publisher
    ..Notably, AP4 is specifically expressed in colonic progenitor and colorectal carcinoma cells. In conclusion, our results indicate that c-MYC employs AP4 to maintain cells in a proliferative, progenitor-like state. ..
  26. Herkert B, Dwertmann A, Herold S, Abed M, Naud J, Finkernagel F, et al. The Arf tumor suppressor protein inhibits Miz1 to suppress cell adhesion and induce apoptosis. J Cell Biol. 2010;188:905-18 pubmed publisher
    ..Our data point to a tumor-suppressive pathway that weakens cell-cell and cell-matrix interactions in response to expression of Arf and that may thereby facilitate the elimination of cells harboring an oncogenic mutation. ..
  27. Huang R, Cheung N, Vider J, Cheung I, Gerald W, Tickoo S, et al. MYCN and MYC regulate tumor proliferation and tumorigenesis directly through BMI1 in human neuroblastomas. FASEB J. 2011;25:4138-49 pubmed publisher
  28. Dominguez Sola D, Ying C, Grandori C, Ruggiero L, Chen B, Li M, et al. Non-transcriptional control of DNA replication by c-Myc. Nature. 2007;448:445-51 pubmed
    ..These findings identify a critical function of c-Myc in DNA replication and suggest a novel mechanism for its normal and oncogenic functions. ..
  29. Grushko T, Dignam J, Das S, Blackwood A, Perou C, Ridderstråle K, et al. MYC is amplified in BRCA1-associated breast cancers. Clin Cancer Res. 2004;10:499-507 pubmed
    ..Thus, we conclude that the aggressive histopathological features of BRCA1-associated tumors are in part due to dysregulated MYC activity. ..
  30. Zhao W, Liu Y, Zhang Q, Wang L, Leboeuf C, Zhang Y, et al. PRDM1 is involved in chemoresistance of T-cell lymphoma and down-regulated by the proteasome inhibitor. Blood. 2008;111:3867-71 pubmed publisher
    ..These results demonstrate the involvement of PRDM1beta in T-cell lymphoma, with possible therapeutic interference by the proteasome inhibitor. ..
  31. Musgrove E, Sergio C, Loi S, Inman C, Anderson L, Alles M, et al. Identification of functional networks of estrogen- and c-Myc-responsive genes and their relationship to response to tamoxifen therapy in breast cancer. PLoS ONE. 2008;3:e2987 pubmed publisher
    ..These functionally-based gene signatures can stratify patients treated with tamoxifen into groups with differing outcome, and potentially identify distinct mechanisms of tamoxifen resistance. ..
  32. Gao P, Tchernyshyov I, Chang T, Lee Y, Kita K, Ochi T, et al. c-Myc suppression of miR-23a/b enhances mitochondrial glutaminase expression and glutamine metabolism. Nature. 2009;458:762-5 pubmed publisher
    ..The unique means by which Myc regulates glutaminase uncovers a previously unsuspected link between Myc regulation of miRNAs, glutamine metabolism, and energy and reactive oxygen species homeostasis. ..
  33. Stearns D, Chaudhry A, Abel T, Burger P, Dang C, Eberhart C. c-myc overexpression causes anaplasia in medulloblastoma. Cancer Res. 2006;66:673-81 pubmed
    ..Because anaplastic changes are often observed in recurrent medulloblastoma, we propose that c-myc dysregulation is involved in the progression of these malignant embryonal neoplasms...
  34. Söderberg O, Gullberg M, Jarvius M, Ridderstråle K, Leuchowius K, Jarvius J, et al. Direct observation of individual endogenous protein complexes in situ by proximity ligation. Nat Methods. 2006;3:995-1000 pubmed
    ..We used this method to show specific regulation of protein-protein interactions between endogenous Myc and Max oncogenic transcription factors in response to interferon-gamma (IFN-gamma) signaling and low-molecular-weight inhibitors. ..
  35. Yuan J, Minter Dykhouse K, Lou Z. A c-Myc-SIRT1 feedback loop regulates cell growth and transformation. J Cell Biol. 2009;185:203-11 pubmed publisher
    ..Overall, our experiments identify a c-Myc-SIRT1 feedback loop in the regulation of c-Myc activity and cellular transformation, supporting/suggesting a role of SIRT1 in tumor suppression. ..
  36. Knoepfler P, Zhang X, Cheng P, Gafken P, McMahon S, Eisenman R. Myc influences global chromatin structure. EMBO J. 2006;25:2723-34 pubmed
    ..This study provides the first evidence for regulation of global chromatin structure by an oncoprotein and may explain the broad effects of Myc on cell behavior and tumorigenesis. ..
  37. Guan Y, Kuo W, Stilwell J, Takano H, Lapuk A, Fridlyand J, et al. Amplification of PVT1 contributes to the pathophysiology of ovarian and breast cancer. Clin Cancer Res. 2007;13:5745-55 pubmed
    ..They also suggest that PVT1-mediated inhibition of apoptosis may explain why amplification of 8q24 is associated with reduced survival duration in patients treated with agents that act through apoptotic mechanisms. ..
  38. Höglund A, Nilsson L, Forshell L, Maclean K, Nilsson J. Myc sensitizes p53-deficient cancer cells to the DNA-damaging effects of the DNA methyltransferase inhibitor decitabine. Blood. 2009;113:4281-8 pubmed publisher
    ..In vivo modeling of Myc-induced lymphoma suggests that decitabine constitutes a potential new drug against lymphoma that would selectively sensitize tumor cells but spare normal tissue. ..
  39. Kim H, Kuwano Y, Srikantan S, Lee E, Martindale J, Gorospe M. HuR recruits let-7/RISC to repress c-Myc expression. Genes Dev. 2009;23:1743-8 pubmed publisher
    ..Our findings suggest a regulatory paradigm wherein HuR inhibits c-Myc expression by recruiting let-7-loaded RISC (RNA miRNA-induced silencing complex) to the c-Myc 3'UTR. ..
  40. Wu X, Cai Z, Lou L, Zhu Y. Expressions of p53, c-MYC, BCL-2 and apoptotic index in human osteosarcoma and their correlations with prognosis of patients. Cancer Epidemiol. 2012;36:212-6 pubmed publisher
    ..We concluded that the expressions of p53, c-MYC, BCL-2 protein and apoptotic index could be used as potential biomarks for predicting the progression and prognosis of osteosarcoma, and for optimizing clinical treatments. ..
  41. Yeh E, Cunningham M, Arnold H, Chasse D, Monteith T, Ivaldi G, et al. A signalling pathway controlling c-Myc degradation that impacts oncogenic transformation of human cells. Nat Cell Biol. 2004;6:308-18 pubmed
    ..Thus, Ras-dependent signalling cascades ensure transient and self-limiting accumulation of c-Myc, disruption of which contributes to human cell oncogenesis. ..
  42. Kiemeney L, Sulem P, Besenbacher S, Vermeulen S, Sigurdsson A, Thorleifsson G, et al. A sequence variant at 4p16.3 confers susceptibility to urinary bladder cancer. Nat Genet. 2010;42:415-9 pubmed publisher
    ..The frequency of rs798766[T] is higher in Ta tumors that carry an activating mutation in FGFR3 than in Ta tumors with wild-type FGFR3. Our results show a link between germline variants, somatic mutations of FGFR3 and risk of UBC. ..
  43. Conacci Sorrell M, Ngouenet C, Eisenman R. Myc-nick: a cytoplasmic cleavage product of Myc that promotes alpha-tubulin acetylation and cell differentiation. Cell. 2010;142:480-93 pubmed publisher
    ..We propose that the cleavage of Myc by calpain abrogates the transcriptional inhibition of differentiation by full-length Myc and generates Myc-nick, a driver of cytoplasmic reorganization and differentiation. ..
  44. Gupta M, Maurer M, Wellik L, Law M, Han J, Ozsan N, et al. Expression of Myc, but not pSTAT3, is an adverse prognostic factor for diffuse large B-cell lymphoma treated with epratuzumab/R-CHOP. Blood. 2012;120:4400-6 pubmed publisher
    ..05), G-CSF (P = .03), and TNF-? (P = .04). pSTAT3 IHC in DLBCL tumors has the potential to identify patients for STAT3 pathway-directed therapy; Myc IHC is a potential marker for inferior EFS in GCB patients. ..
  45. Shi J, Liu W, Zhang T, Wang S, Lin X, Li J, et al. The enforced expression of c-Myc in pig fibroblasts triggers mesenchymal-epithelial transition (MET) via F-actin reorganization and RhoA/Rock pathway inactivation. Cell Cycle. 2013;12:1119-27 pubmed publisher
    ..Taken together, these findings demonstrate, for the first time, that the enforced expression of c-Myc in fibroblasts can trigger MET, to which cytoskeleton depolymerization and RhoA/Rock pathway inactivation contribute. ..
  46. Gregory M, Qi Y, Hann S. Phosphorylation by glycogen synthase kinase-3 controls c-myc proteolysis and subnuclear localization. J Biol Chem. 2003;278:51606-12 pubmed
    ..Finally, we show that Thr-58 phosphorylation alters the subnuclear localization of c-Myc, enhancing its localization to discrete nuclear bodies together with GSK-3. ..
  47. Cairo S, Wang Y, de Reynies A, Duroure K, Dahan J, Redon M, et al. Stem cell-like micro-RNA signature driven by Myc in aggressive liver cancer. Proc Natl Acad Sci U S A. 2010;107:20471-6 pubmed publisher
    ..Our data argue that Myc-driven reprogramming of miR expression patterns contributes to the aggressive phenotype of liver tumors originating from hepatic progenitor cells. ..
  48. Blackwood E, Eisenman R. Max: a helix-loop-helix zipper protein that forms a sequence-specific DNA-binding complex with Myc. Science. 1991;251:1211-7 pubmed
    ..These results suggest that Myc family proteins undergo a restricted set of interactions in the cell and may belong to the more general class of eukaryotic DNA-binding transcription factors. ..
  49. Green T, Young K, Visco C, Xu Monette Z, Orazi A, Go R, et al. Immunohistochemical double-hit score is a strong predictor of outcome in patients with diffuse large B-cell lymphoma treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone. J Clin Oncol. 2012;30:3460-7 pubmed
    ..The immunohistochemical DHS defined a large subset of DLBCLs with double-hit biology and was strongly associated with poor outcome in patients treated with R-CHOP. ..
  50. Albihn A, Lovén J, Ohlsson J, Osorio L, Henriksson M. c-Myc-dependent etoposide-induced apoptosis involves activation of Bax and caspases, and PKCdelta signaling. J Cell Biochem. 2006;98:1597-614 pubmed
    ..Taken together, these findings suggest that Bax and caspase activation, together with PKCdelta signaling are involved in c-Myc-dependent etoposide-induced apoptosis. ..
  51. Gordan J, Bertout J, Hu C, Diehl J, Simon M. HIF-2alpha promotes hypoxic cell proliferation by enhancing c-myc transcriptional activity. Cancer Cell. 2007;11:335-47 pubmed
    ..Enhanced c-Myc activity likely contributes to HIF-2alpha-mediated neoplastic progression following loss of the VHL tumor suppressor and influences the behavior of hypoxic tumor cells. ..
  52. An J, Yang D, Xu Q, Zhang S, Huo Y, Shang Z, et al. DNA-dependent protein kinase catalytic subunit modulates the stability of c-Myc oncoprotein. Mol Cancer. 2008;7:32 pubmed publisher
    ..Our results suggest DNA-PKcs a novel biological role beyond its DNA repair function. ..
  53. Alles M, Gardiner Garden M, Nott D, Wang Y, Foekens J, Sutherland R, et al. Meta-analysis and gene set enrichment relative to er status reveal elevated activity of MYC and E2F in the "basal" breast cancer subgroup. PLoS ONE. 2009;4:e4710 pubmed publisher
  54. Hydbring P, Bahram F, Su Y, Tronnersjö S, Högstrand K, von der Lehr N, et al. Phosphorylation by Cdk2 is required for Myc to repress Ras-induced senescence in cotransformation. Proc Natl Acad Sci U S A. 2010;107:58-63 pubmed publisher
    ..Finally, our findings highlight that pharmacological inhibition of Cdk2 activity is a potential therapeutical principle for cancer therapy, in particular for tumors with activated Myc or Ras. ..
  55. Zhang Q, Spears E, Boone D, Li Z, Gregory M, Hann S. Domain-specific c-Myc ubiquitylation controls c-Myc transcriptional and apoptotic activity. Proc Natl Acad Sci U S A. 2013;110:978-83 pubmed publisher
    ..Therapeutic strategies could be developed to activate this intrinsic apoptotic activity of c-Myc to inhibit tumorigenesis. ..
  56. Weber A, Liu J, Collins I, Levens D. TFIIH operates through an expanded proximal promoter to fine-tune c-myc expression. Mol Cell Biol. 2005;25:147-61 pubmed
    ..This helps to suppress the intrinsic noise of transcription and to ensure the steady transcriptional output of c-myc necessary for cellular homeostasis. ..
  57. Zhang X, DeSalle L, Patel J, Capobianco A, Yu D, Thomas Tikhonenko A, et al. Metastasis-associated protein 1 (MTA1) is an essential downstream effector of the c-MYC oncoprotein. Proc Natl Acad Sci U S A. 2005;102:13968-73 pubmed
    ..These data implicate MTA1 and the Mi-2/NURD complex as one of the first downstream targets of c-MYC function that are essential for the transformation potential of c-MYC. ..
  58. Bhandari D, Seo K, Jung J, Kim H, Yang S, Kang K. The regulatory role of c-MYC on HDAC2 and PcG expression in human multipotent stem cells. J Cell Mol Med. 2011;15:1603-14 pubmed publisher
    ..From this finding, it can be concluded that c-MYC plays a vital role in cell proliferation and differentiation via chromosomal modification...
  59. Iijima S, Teraoka H, Date T, Tsukada K. DNA-activated protein kinase in Raji Burkitt's lymphoma cells. Phosphorylation of c-Myc oncoprotein. Eur J Biochem. 1992;206:595-603 pubmed
    ..Phosphopeptide mapping and phosphoamino acid analysis indicated that DNA-PK phosphorylates c-Myc in vitro at several serine residues. ..
  60. Seth A, Alvarez E, Gupta S, Davis R. A phosphorylation site located in the NH2-terminal domain of c-Myc increases transactivation of gene expression. J Biol Chem. 1991;266:23521-4 pubmed
    ..These data indicate that the c-Myc transcriptional activation domain may be a direct target of signal transduction pathways. ..
  61. Elliott K, Sakamuro D, Basu A, Du W, Wunner W, Staller P, et al. Bin1 functionally interacts with Myc and inhibits cell proliferation via multiple mechanisms. Oncogene. 1999;18:3564-73 pubmed
    ..These findings supported functional interaction between Myc and Bin1 in cells and indicated that Bin1 could inhibit malignant cell growth through multiple mechanisms. ..
  62. Korz C, Pscherer A, Benner A, Mertens D, Schaffner C, Leupolt E, et al. Evidence for distinct pathomechanisms in B-cell chronic lymphocytic leukemia and mantle cell lymphoma by quantitative expression analysis of cell cycle and apoptosis-associated genes. Blood. 2002;99:4554-61 pubmed
    ..In contrast, in MCL the impairment of apoptosis induction seems to play a minor role, whereas most expression data indicate an enhancement of cell proliferation. ..
  63. Dose M, Khan I, Guo Z, Kovalovsky D, Krueger A, von Boehmer H, et al. c-Myc mediates pre-TCR-induced proliferation but not developmental progression. Blood. 2006;108:2669-77 pubmed
  64. Koch H, Zhang R, Verdoodt B, Bailey A, Zhang C, Yates J, et al. Large-scale identification of c-MYC-associated proteins using a combined TAP/MudPIT approach. Cell Cycle. 2007;6:205-17 pubmed
    ..Furthermore, this first comprehensive description of the c-MYC-associated sub-proteome will facilitate further studies aimed to elucidate the biology of c-MYC. ..
  65. Lee S, Hu L, Gonzalez Navajas J, Seo G, Shen C, Brick J, et al. ERK activation drives intestinal tumorigenesis in Apc(min/+) mice. Nat Med. 2010;16:665-70 pubmed publisher
    ..Our data reveal a new facet of oncogene-environment interaction, in which microflora-induced TLR activation regulates oncogene expression and related IEC tumor growth in a susceptible host...
  66. Barrans S, Crouch S, Smith A, Turner K, Owen R, Patmore R, et al. Rearrangement of MYC is associated with poor prognosis in patients with diffuse large B-cell lymphoma treated in the era of rituximab. J Clin Oncol. 2010;28:3360-5 pubmed publisher
    ..In DLBCL, rearrangement of MYC is rarely found as the sole genetic abnormality and the poor prognosis of these patients is likely to reflect a synergistic effect alongside deregulation of BCL6 or BCL2. ..
  67. Zhang X, Zhao X, Fiskus W, Lin J, Lwin T, Rao R, et al. Coordinated silencing of MYC-mediated miR-29 by HDAC3 and EZH2 as a therapeutic target of histone modification in aggressive B-Cell lymphomas. Cancer Cell. 2012;22:506-523 pubmed publisher
    ..These findings define a MYC-mediated miRNA repression mechanism, shed light on MYC lymphomagenesis mechanisms, and reveal promising therapeutic targets for aggressive B-cell malignancies. ..
  68. Brenner C, Deplus R, Didelot C, Loriot A, Viré E, De Smet C, et al. Myc represses transcription through recruitment of DNA methyltransferase corepressor. EMBO J. 2005;24:336-46 pubmed
    ..Furthermore, these findings suggest that targeting of DNA methyltransferases by transcription factors is a wide and general mechanism for the generation of specific DNA methylation patterns within a cell. ..
  69. Zhang K, Faiola F, Martinez E. Six lysine residues on c-Myc are direct substrates for acetylation by p300. Biochem Biophys Res Commun. 2005;336:274-80 pubmed
    ..Our results further indicate that p300 can acetylate DNA-bound Myc:Max complexes and that acetylated Myc:Max heterodimers efficiently interact with Miz-1. ..
  70. Cowling V, Cole M. E-cadherin repression contributes to c-Myc-induced epithelial cell transformation. Oncogene. 2007;26:3582-6 pubmed
    ..E-cadherin expression is repressed by a post-transcriptional mechanism in cells expressing c-Myc. Furthermore, E-cadherin repression is necessary for c-Myc-induced cell transformation. ..
  71. Kokai E, Voss F, Fleischer F, Kempe S, Marinkovic D, Wolburg H, et al. Myc regulates embryonic vascular permeability and remodeling. Circ Res. 2009;104:1151-9 pubmed publisher
    ..Thus, the net outcome of an excess of vascular endothelial growth factor-A and angiopoietin-2 in the face of an elevated cellular turnover appears to be a defect in vascular integrity. ..
  72. Fan J, Zeller K, Chen Y, Watkins T, Barnes K, Becker K, et al. Time-dependent c-Myc transactomes mapped by Array-based nuclear run-on reveal transcriptional modules in human B cells. PLoS ONE. 2010;5:e9691 pubmed publisher
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