Emerging roles of E2Fs in cancer: an exit from cell cycle control
By Hui-Zi Chen, Shih-Yin Tsai, Gustavo Leone. Nature Reviews. Cancer, 2009
1,012 citations recorded by the source corpus.
Mutations of the retinoblastoma tumour suppressor gene (RB1) or components regulating the RB pathway have been identified in almost every human malignancy. The E2F transcription factors function in cell cycle control and are intimately regulated by RB. Studies of model organisms have revealed conserved functions for E2Fs during development, suggesting that the cancer-related proliferative roles of E2F family members represent a recent evolutionary adaptation. However, given that some human tumours have concurrent RB1 inactivation and E2F amplification and overexpression, we propose that there are alternative tumour-promoting activities for the E2F family, which are independent of cell cycle regulation.
Subfields: Cancer Research, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/2681ae18a6a34a2a80ae2d3b83c9a768393c7545
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Citations in the corpus
- ISMARA: automated modeling of genomic signals as a democracy of regulatory motifs (2014, neutral): “5[42], NF-Y[43], YY1[44], TFCP2[45], and the SMAD TFs[46].”
- Cyclin D as a therapeutic target in cancer (2011, background): “The simple model in which RB phosphorylation by CDKs, including cyclin D–CDK4/CDK6, promotes the activation of E2F-responsive genes that are necessary for DNA synthesis has subsequently been elaborated to take into account factors such as combinatorial interactions between RB family proteins and var”
- Control of the senescence-associated secretory phenotype by NF-κB promotes senescence and enhances chemosensitivity. (2011, background): “Indeed, a more detailed analysis of E2F target genes, which are negatively regulated by RB (Chen et al. 2009), indicates that NF-kB has little impact on their expression (Supplemental Fig.”