ArticleOncogene2001
Sequence-specific enhancer binding protein is responsible for the differential expression of ERT/ESX/ELF-3/ESE-1/jen gene in human gastric cancer cell lines: Implication for the loss of TGF-beta type II receptor expression.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 22 citations in OpenAlex.
- ELF-3 and TSC-1 as potential markers of recurrence in low-risk non-muscle-invasive bladder cancer.BMC cancer · 2026Article
- Involvement of Elf3 on Smad3 activation-dependent injuries in podocytes and excretion of urinary exosome in diabetic nephropathy.PloS one · 2019Article
- Transcriptome profiling of cancer tissues in Chinese patients with gastric cancer by high-throughput sequencing.Oncology letters · 2018Article
- Moonlighting proteins in cancer.Cancer letters · 2016Review
- Whole-genome sequencing and comprehensive molecular profiling identify new driver mutations in gastric cancer.Nature genetics · 2014Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
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Abstract
Transcriptional repression of the TGF-beta type II receptor (RII) is one of the mechanisms leading to TGF-beta resistance. The newly identified epithelium-specific ets transcription factor ERT/ESX/ELF-3/ESE-1/jen binds to the TGF-beta RII promoter and induces promoter activity. The human gastric cancer cell lines, which show undetectable level of TGF-beta RII mRNA, do not express ERT mRNA. To study the molecular mechanisms of loss of ERT expression, we have cloned and characterized the human ERT promoter. DNA transfection experiments and electrophoretic mobility shift assays have revealed the existence of a distinct enhancer element (-186 to -177) which we named ESE (ERT promoter specific element). Deletion of the ESE markedly decreased expression of the target gene. ESE interacts with two distinct nuclear protein complexes, at least one of which appears to be inactivated in a cell line which does not express the ERT mRNA, compared to a cell line expressing the ERT mRNA. These results suggest the possibility that inactivation of the sequence-specific DNA binding protein to the region from -186 to -177 contributes to the loss of ERT expression, leading to the loss of TGF-beta type II receptor mRNA in human gastric cancer cell lines.
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