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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.
Oncogene. 2001 Mar 08; 20(10):1235-45.O

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.

Authors+Show Affiliations

Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, Bethesda, MD 20892-5055, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11313868

Citation

Park, S H., et al. "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." Oncogene, vol. 20, no. 10, 2001, pp. 1235-45.
Park SH, Kim YS, Park BK, et al. 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. Oncogene. 2001;20(10):1235-45.
Park, S. H., Kim, Y. S., Park, B. K., Hougaard, S., & Kim, S. J. (2001). 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. Oncogene, 20(10), 1235-45.
Park SH, et al. 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. Oncogene. 2001 Mar 8;20(10):1235-45. PubMed PMID: 11313868.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Park,S H, AU - Kim,Y S, AU - Park,B K, AU - Hougaard,S, AU - Kim,S J, PY - 2000/10/26/received PY - 2000/12/26/revised PY - 2001/01/04/accepted PY - 2001/4/21/pubmed PY - 2001/5/22/medline PY - 2001/4/21/entrez SP - 1235 EP - 45 JF - Oncogene JO - Oncogene VL - 20 IS - 10 N2 - 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. SN - 0950-9232 UR - https://www.unboundmedicine.com/medline/citation/11313868/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_ L2 - https://doi.org/10.1038/sj.onc.1204227 DB - PRIME DP - Unbound Medicine ER -