The ETS family of oncogenic transcription factors in solid tumours

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Abstract

Initially identified more than 30 years ago, the ETS family of transcription factors has been found to take part in all steps of tumorigenesis. This Review discusses the different mechanisms of ETS activation and the oncogenic implications of this activation, as well as how to target ETS factors in cancer treatment.

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Mutant p53 in Cancer: New Functions and Therapeutic Opportunities

Patricia A.J. Muller, Karen H. Vousden (2014)

Many different types of cancer show a high incidence of TP53 mutations, leading to the expression of mutant p53 proteins. There is growing evidence that these mutant p53s have both lost wild-type p53 tumor suppressor activity and gained functions that help to contribute to malignant progression. Understanding the functions of mutant p53 will help in the development of new therapeutic approaches that may be useful in a broad range of cancer types.

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Gene fusion with an ETS DNA-binding domain caused by chromosome translocation in human tumours.

O Delattre, J Zucman, B Plougastel … (1992)

Ewing's sarcoma and related subtypes of primitive neuroectodermal tumours share a recurrent and specific t(11;22) (q24;q12) chromosome translocation, the breakpoints of which have recently been cloned. Phylogenetically conserved restriction fragments in the vicinity of EWSR1 and EWSR2, the genomic regions where the breakpoints of chromosome 22 and chromosome 11 are, respectively, have allowed identification of transcribed sequences from these regions and has indicated that a hybrid transcript might be generated by the translocation. Here we use these fragments to screen human complementary DNA libraries to show that the translocation alters the open reading frame of an expressed gene on chromosome 22 gene by substituting a sequence encoding a putative RNA-binding domain for that of the DNA-binding domain of the human homologue of murine Fli-1.

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Genome-wide analysis of ETS-family DNA-binding in vitro and in vivo

Gong-Hong Wei, Gwenael Badis, Michael F. Berger … (2010)

Members of the large ETS family of transcription factors (TFs) have highly similar DNA-binding domains (DBDs)—yet they have diverse functions and activities in physiology and oncogenesis. Some differences in DNA-binding preferences within this family have been described, but they have not been analysed systematically, and their contributions to targeting remain largely uncharacterized. We report here the DNA-binding profiles for all human and mouse ETS factors, which we generated using two different methods: a high-throughput microwell-based TF DNA-binding specificity assay, and protein-binding microarrays (PBMs). Both approaches reveal that the ETS-binding profiles cluster into four distinct classes, and that all ETS factors linked to cancer, ERG, ETV1, ETV4 and FLI1, fall into just one of these classes. We identify amino-acid residues that are critical for the differences in specificity between all the classes, and confirm the specificities in vivo using chromatin immunoprecipitation followed by sequencing (ChIP-seq) for a member of each class. The results indicate that even relatively small differences in in vitro binding specificity of a TF contribute to site selectivity in vivo.

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Journal

Title: Nature Reviews Cancer

Abbreviated Title: Nat Rev Cancer

Publisher: Springer Nature

ISSN (Print): 1474-175X

ISSN (Electronic): 1474-1768

Publication date Created: April 28 2017

Publication date (Print): April 28 2017

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Article

DOI: 10.1038/nrc.2017.20

PubMed ID: 28450705

SO-VID: 9d337747-7eab-42cf-a970-3ca8d1c8118b

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The ETS family of oncogenic transcription factors in solid tumours

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Most cited references 138

Mutant p53 in Cancer: New Functions and Therapeutic Opportunities

Gene fusion with an ETS DNA-binding domain caused by chromosome translocation in human tumours.

Genome-wide analysis of ETS-family DNA-binding in vitro and in vivo

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