Differential modulation of Myb family genes by Ets-2

Kang, Anthony D.; Park, Gyeongsin; Kim, Yeul Hong; Oh, Il‐Hoan

doi:10.1038/sj.onc.1207537

Cited by 1 publication

(1 citation statement)

References 21 publications

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“…Binding sites for Elf-1 have been identified in the promoters of several important lymphoid-specific genes such as IL-3 [23] and GM-CSF [23]. ETS-2 has a distinct tissue-specific expression pattern [25,26]. Deficiency of the ETS-2 gene leads to day E8.5 embryonic lethality, with defects in extraembryonic tissue gene expression and function and the failure of ectoplacental cone proliferation [27].…”

Section: The Direct In Situ Binding Of Ets-2 And/or Elf-1 To Their Comentioning

confidence: 99%

Transcription of the putative tumor suppressor gene HCCS1 requires binding of ETS-2 to its consensus near the transcription start site

Zhu

Wang

et al. 2006

Cell Res

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The hepatocellular carcinoma suppressor 1 (HCCS1) gene was identified by both positional cloning from a predominant region of loss of heterozygosity (17p13.3) in liver cancer and by functional screening for genes affecting cell proliferation in large-scale transfection assays. Its overexpression results in inhibition of cell proliferation in cell culture and tumor growth in nude mice. To understand its transcription regulation, the promoter architecture has been dissected in detail. The major start of transcription was mapped by primer extension to a C residue, 177 nucleotides upstream of the ATG codon. By assessing the promoter activity of a set of linker-scanning mutants of the minimal promoter (-60 to +148 region) in a transient transfection assay, we found that the +1 to + 40 region is critical to HCCS1 gene transcription, containing binding sites for transcription factors NF-κB (-21 to +7 and +40 to +26), p53 (+29 to +9) and ETS (+4 to +20 and +23 to +39). Biochemical and molecular analyses revealed that the ETS transcription factors ETS-2 and Elf-1 bind to the two ETS sites in situ and contribute significantly to the transcriptionally active state of the HCCS1 gene, while NF-κB, p53 and two other members of the ETS family (ETS-1 and NERF2) appear to play little role. Our observations provide insight into the mechanistic aspects of HCCS1 transcription regulation.

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