Expression analysis with oligonucleotide microarrays reveals that MYC regulates genes involved in growth, cell cycle, signaling, and adhesion.

By Hilary A. Coller, C. Grandori, Pablo Tamayo, T. Colbert, Eric S. Lander, R. Eisenman, Todd R. Golub. Proceedings of the National Academy of Sciences of the United States of America, 2000

865 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/4cb4f63b5ad13375acdbadb269add5310d5510ba

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Citations in the corpus

HIF-2alpha promotes hypoxic cell proliferation by enhancing c-myc transcriptional activity. (2007, background): “Of note, hypoxic culture for 4 or 20 hr correlated with a substantial decrease in c-Myc coprecipitation with Sp1, Miz1, and Max in HCT116 cells and an increase in c-Myc coprecipitation with these proteins in WT8 cells, albeit less dramatically than the decrease seen in HCT116 cells (Figure 6A).”
Module map of stem cell genes guides creation of epithelial cancer stem cells. (2008, methodology): “We similarly observed induction of the ESC-like module by c-Myc in primary human fibroblasts and a nontransformed breast epithelial cell line (Figures S2A and S2B; Adler et al., 2006; Coller et al., 2000).”
Lost in transcription: p21 repression, mechanisms, and consequences. (2005, background): “A study using microarray analysis has implicated p21 as one of the major targets of c-Myc repression (19).”
Inflammatory Myofibroblastic Tumor: Comparison of Clinicopathologic, Histologic, and Immunohistochemical Features Including ALK Expression in Atypical and Aggressive Cases (2007, background): “Although the functional consequences of c-Myc expression in ALCL are unclear, c-Myc is considered an oncogenic switch.(13,17) In IMT, nuclear c-Myc expression was found in 91% of cases tested, but there were no differences among the ALK-positive and negative subgroups.”
Shape-dependent control of cell growth, differentiation, and apoptosis: switching between attractors in cell regulatory networks. (2000, background): “Even activation of a signaling molecule far down in the mitogenic pathway (the c-myc transcription factor) induced expression of 27 different genes [7].”
Myc-driven murine prostate cancer shares molecular features with human prostate tumors. (2003, background): “…cancer will be possible by futurefrom expansion of a particular cell type) or specifically in prostate tumorigenesis or Myc-driven tumorigenesis (Coller et al., 2000). comparison of the Myc-driven tumors to other mouse prostate CANCER CELL : SEPTEMBER 2003 231 cancer models (Wu et al., 2003…”
The ERK1/2 mitogen-activated protein kinase pathway as a master regulator of the G1- to S-phase transition (2007, background): “Among the best-defined c-Myc targets that function directly in cell cycle control are cyclin D2 (Bouchard et al., 1999; Coller et al., 2000), Cdk4 (Hermeking et al.”
E2Fs regulate the expression of genes involved in differentiation, development, proliferation, and apoptosis. (2001, background): “We also observed significant bias toward genes regulated by p53 (Zhao et al. 2000), c-Myc (Coller et al. 2000), activated Ras (Zuber et al. 2000), and replicative senescence (Shelton et al. 1999).”
c-Myc and Cancer Metabolism (2012, positive): “Large-scale studies of gene expression in rat and human systems first suggested that cMyc overexpression can induce nuclearly encoded mitochondrial genes (24, 25, 29).”
Targeting lactate metabolism for cancer therapeutics. (2013, background): “Increased levels of MCT1 in tumors expressing high levels of MYC have also been noted in expression arrays (78, 79), and genome-wide chromatin immunoprecipitation analyses of MYC binding indicate that MYC binds to the MCT1 promoter of both normal and cancer cell lines (80).”
MicroRNA-10a binds the 5'UTR of ribosomal protein mRNAs and enhances their translation. (2008, background): “Both MYC and NMYC directly bind and transcriptionally activate a cohort of genes encompassing both rRNA genes, RP genes, and other translational regulators (Boon et al., 2001; Coller et al., 2000; Grandori et al., 2005).”
c-Myc can induce DNA damage, increase reactive oxygen species, and mitigate p53 function: a mechanism for oncogene-induced genetic instability. (2002, background): “…with previous reports, c-Myc activated the expression of genes involved in multiple physiological functions, including basal metabolism, nucleotide biosynthesis, control of cell cycle progression, and apoptosis (Coller et al., 2000; Dang, 1999; O’Hagan et al., 2000; Packham and Cleveland, 1994).”