MYC on the Path to Cancer

By C. V. Dang. Cell, 2012

3,217 citations recorded by the source corpus.

The MYC oncogene contributes to the genesis of many human cancers. Recent insights into its expression and function have led to new cancer therapeutic opportunities. MYC’s activation by bromodomain proteins could be inhibited by drug-like molecules, resulting in tumor inhibition in vivo. Tumor growth can also be curbed by pharmacologically uncoupling bioenergetic pathways involving glucose or glutamine metabolism from Myc-induced cellular biomass accumulation. Other approaches to halt Myc on the path to cancer involve targeting Myc-Max dimerization or Myc-induced microRNA expression. Here the richness of our understanding of MYC is reviewed, highlighting new biological insights and opportunities for cancer therapies.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/66c771874a9e83c4bc7084f1297f18930f9da71a

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In Molecular Biology

Citations in the corpus

Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “Importantly, targeting the PI3K-AKT-mTOR network can result in tumour resistance due to MYC activation [434].”
Metabolic reprogramming and epigenetic modifications on the path to cancer (2021, background): “For example, in addition to regulating glucose, glutamine and serine metabolism at the transcriptional level (Gao et al., 2009; Stine et al., 2015; Sun et al., 2015; Wu et al., 2017), cMyc increases SDHA (succinate dehydrogenase complex, subunit A) acetylation by promoting SKP2 (S-phase kinaseassoci”
THE HISTONE DEACETYLASE SIRT6 IS A NOVEL TUMOR SUPPRESSOR THAT CONTROLS CANCER METABOLISM (2012, positive): “Beyond ribosome biosynthesis, MYC regulates glucose and glutamine metabolism (Dang, 2012).”
Transcriptional Amplification in Tumor Cells with Elevated c-Myc (2012, positive): “Mitogenic growth factor signaling inducesMYC expression, and c-Myc is thought to enhance transcription of proliferation-associated genes (Dang, 2012; Eilers and Eisenman, 2008; Meyer and Penn, 2008).”
MYC, Metabolism, and Cancer. (2015, background): “Regardless of the exact function of MYC in regulating gene expression, studies to date support the notion that activation of MYC results in a genomic program that promotes ribosome biogenesis, cell growth, and subsequently cell proliferation (8, 59).”
An Integrated Metabolic Atlas of Clear Cell Renal Cell Carcinoma (2016, positive): “Furthermore, it is now established that key oncogenes such asMYC and KRAS can reorganize cellular metabolism to support tumor fitness (Commisso et al., 2013; Dang, 2012).”
Metabolic Plasticity in Stem Cell Homeostasis and Differentiation (2012, positive): “Chromatin modifiers, such as polycomb repressor complexes, which promote pluripotency, also targetmetabolic enzymeswithin their active gene sets (Brookes et al., 2012; Dang, 2012).”
The Warburg effect in tumor progression: Mitochondrial oxidative metabolism as an anti-metastasis mechanism (2014, background): “Myc is an oncogenic transcription factor involved in the regulation of cell metabolism and cell proliferation, and is commonly deregulated in cancer [58].”
Autophagy in malignant transformation and cancer progression (2015, positive): “…viral oncogene homolog (MYC), v-myc avian myelocytomatosis viral oncogene lung carcinoma-derived homolog (MYCL) and v-myc avian myelocytomatosis viral oncogene neuroblastoma derived homolog (MYCN) are the major effectors of the mitogenic MAPK\ERK signal transduction cascade (Dang, 2012).”