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REGULAR ARTICLES Cell Research (2002); 12(5-6):339-352 The promoter analysis of the human C17orf25 gene, a novel chromosome 17p13.3 gene Jian Ying GUO*, Jian XU*, Da Qin MAO, Li Li FU, Jian Ren GU, Jing De ZHU** The State-Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ln 2200/25, Xie-Tu Road, Shanghai 200032, China Received Sep-12-20027nbsp; Revised Oct-21-2002 Accepted Nov-5-2002 *Both authors have contributed equally to this work
Abbreviations used in this paper: LOH, loss of heterozygosity; HCC, hepatocellular carcinoma; SP1, specificity protein 1; AP-1, activating protein 1; RT-PCR, reverse transcription-PCR; EMSA, electrophoretic mobility shift assay; IVT, the in vitro transcription/translation.
The human C17orf25 gene (Accession No. AF177342) is one of thirteen genes cloned from a region displaying a high score of loss of heterozygosity within chromosome 17p13.3 in human hepatocellular carcinoma in China[1]. To unveil the underlying mechanisms for the transcription regulation of this gene and understand its implication to the hepatocellular carcinogenesis, we looked into the relevant aspects by both bioinformatic and experimental executions. We found: 1, The abundant expression of the C17orf25 gene was evident in all the cell lines and tissue samples tested, showing little hepatoma-selectivity; 2, Its transcription starts at a single site, locating at -60 from the translation initiation codon; 3, A 58 bp fragment containing the transcription start, extending from -112 to -55, represents the minimal promoter; 4, The consensus sequence within this fragment recognized by SP1 contributes predominantly to the activity of the minimal promoter; 5, The bioinformatic analysis suggests that the C17orf25 gene may encode a protein in the family of the glyoxalase. Our data has provided some deep insight into both function and regulation of the C17orf25 gene in the context of the normal liver and hepatocellular carcinoma. Key words: C17orf25 gene, SP1, transcription regulation, chromosome 17p13.3.
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