Abstract
The ETS transcription factors regulate expression of genes involved in normal cell development, proliferation, differentiation, angiogenesis, and apoptosis, consisting of 28 family members in humans. Dysregulation of these transcription factors facilitates cell proliferation in cancers, and several members participate in invasion and metastasis by activating gene transcription. ETS1 and ETS2 are the founding members of the ETS family and regulate transcription by binding to ETS sequences. They are both involved in oncogenesis and tumor suppression depending on the biological situations used. The essential roles of ETS proteins in human telomere maintenance have been suggested, which have been linked to creation of new Ets binding sites. Recently, preferential binding of ETS2 to gain-of-function mutant p53 and ETS1 to wild type p53 (WTp53) has been suggested, raising the tumor promoting role for the former and tumor suppressive role for the latter. The oncogenic and tumor suppressive functions of ETS1 and 2 proteins have been discussed.
Highlights
The oncogene v-ets was originally discovered as a component of a chimeric gene along with a truncated v-myb gene, present in the genome of E26, an avian leukosis virus (Figure 1A) [1,2,3]
The human ETS factors are classified into 11 subgroups based upon ETS domain sequence homology: ETS1/2, ERG, PEA3 (ETV1/4/5), TCF (ELK1/3/4), GABP (GABPA: GA [purine] -binding protein alpha chain), ELF1/2/4, SPI1 (SPI1/B/C), TEL (ETV6/7), ERF (ERF, ETV3, ETV3L), FLI1 and FEV [4]
The chimeric gene responsible for acute myeloid leukemia was did not contain ETS, the ETS family ERG1 was situated just proximal to ETS2 at 21q22.3 [29,30] (Figure 1B)
Summary
The oncogene v-ets was originally discovered as a component of a chimeric gene along with a truncated v-myb gene, present in the genome of E26, an avian leukosis virus (Figure 1A) [1,2,3]. The ETS family of transcription factors have the conserved primary sequence of their DNA-binding domains (Figure 1; ETS1/2, ERG, and FLI1 are shown). The chimeric gene responsible for acute myeloid leukemia was did not contain ETS, the ETS family ERG1 was situated just proximal to ETS2 at 21q22.3 [29,30] (Figure 1B). They found that the ERG1 gene was translocated from chromosome 21 to chromosome 8 in the t(8;21)(q22;q22) [30]. The newly described germline and recurrent somatic mutations in melanoma [35] and other cancers [36] in the TERT promoter that create de novo ETS/
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