Dataset Information

HemoPDB: Hematopoiesis Promoter Database, an information resource of transcriptional regulation in blood cell development.

ABSTRACT: Hematopoiesis describes the process of the normal formation and development of blood cells, involving both proliferation and differentiation from stem cells. Abnormalities in this developmental program yield blood cell diseases, such as leukemia. Although, in recent years, extensive molecular research in normal hematopoietic development has characterized transcription factors and their binding sites in the target gene promoters, the information generated is highly fragmented. In order to integrate this important regulatory information with the corresponding genomic sequences, we have developed a new database called Hematopoiesis Promoter Database (HemoPDB). HemoPDB is a comprehensive resource focused on transcriptional regulation during hematopoietic development and associated aberrances that result in malignancy. HemoPDB (version 1.0) contains 246 promoter sequences and 604 experimentally known cis-regulatory elements of 187 different transcription factors, with links to published references. Orthologous promoters from different species are linked with each other and displayed in the same database record, accompanied by a visual image of the promoters and corresponding annotations of cis-regulatory elements. HemoPDB may be searched for the promoter of a specific gene, transcription factors and target genes, and genes that are expressed in a certain cell type or lineage, through a user-friendly web interface at http://bioinformatics.med.ohio-state.edu/HemoPDB. Links to the documentation and other technical details are provided on this website.

SUBMITTER: Pohar TT

PROVIDER: S-EPMC308790 | biostudies-literature | 2004 Jan

REPOSITORIES: biostudies-literature

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HemoPDB: Hematopoiesis Promoter Database, an information resource of transcriptional regulation in blood cell development.

Pohar Twyla T TT Sun Hao H Davuluri Ramana V RV

Nucleic acids research 20040101 Database issue

Hematopoiesis describes the process of the normal formation and development of blood cells, involving both proliferation and differentiation from stem cells. Abnormalities in this developmental program yield blood cell diseases, such as leukemia. Although, in recent years, extensive molecular research in normal hematopoietic development has characterized transcription factors and their binding sites in the target gene promoters, the information generated is highly fragmented. In order to integra ...[more]

PMID: 14681365

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Project description:BACKGROUND: MYCT1, previously named MTLC, is a novel candidate tumor suppressor gene. MYCT1 was cloned from laryngeal squamous cell cancer (LSCC) and has been found to be down-regulated in LSCC; however, the regulatory details have not been fully elucidated. METHODS: Here, we sought to investigate the methylation status of the CpG islands of MYCT1 and mRNA levels by bisulfite-specific PCR (BSP) based on sequencing restriction enzyme digestion, reverse transcription and real-time quantitative polymerase chain reaction (RQ-PCR). The function of specific sites in the proximal promoter of MYCT1 in LSCC was measured by transient transfection, luciferase assays, electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation assay (ChIP). RESULTS: The results suggested hypermethylation of 12 CpG sites of the promoter in both laryngeal cancer tissues and the laryngeal cancer line Hep-2 cell. The hypermethylation of the site CGCG (-695 to -692), which has been identified as the c-Myc binding site, was identified in laryngeal cancer tissues (59/73) compared to paired mucosa (13/73); in addition, statistical analysis revealed that the methylation status of this site significantly correlated with cancer cell differentiation(p?<?0.01). The mRNA level of MYCT1 increased in Hep-2 cells treated with 5-aza-C (p?<?0.01). The luciferase activity from mutant transfectants pGL3-MYCT1m (-852/+12, mut-695-C?>?A, mut-693-C?>?G) was significantly reduced compared with the wild type pGL3-MYCT1 (-852/+12), while the luciferase activity from wild transfectants pGL3-MYCT1 (-852/+12) rose after 5-aza treatment in Hep-2 cells. Finally, EMSA and ChIP confirmed that the methylation of the CGCG (-695 to -692) site prevented c-Myc from binding of the site and demethylation treatment of the 5' flanking region of MYCT1 by 5-aza induced the increased occupation of the core promoter by c-Myc (p?<?0.01). CONCLUSION: In summary, this study concluded that hypermethylation contributed to the transcriptional down-regulation of MYCT1 and could inhibit cancer cell differentiation in LSCC. DNA methylation of the CGCG site (-695 to -692) of MYCT1 altered the promoter activity by interfering with its binding to c-Myc in LSCC. Epigenetic therapy of reactivating MYCT1 by 5-aza should be further evaluated in clinical trails of LSCC.

Dataset Information

HemoPDB: Hematopoiesis Promoter Database, an information resource of transcriptional regulation in blood cell development.

Publications

HemoPDB: Hematopoiesis Promoter Database, an information resource of transcriptional regulation in blood cell development.

Similar Datasets

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