RESUMO
Head-to-head genes with a short distance between their transcription start sites may constitute up to 10% of all genes in the genomes of various species. It was hypothesized that this intergenic space may represent bidirectional promoters which are able to initiate transcription of both genes, but the true bidirectionality was proved only for a few of them. We present experimental evidence that, according to several criteria, a 269 bp region located between the PSENEN and U2AF1L4 human genes is a genuine bidirectional promoter regulating a concerted divergent transcription of these genes. Concerted transcription of PSENEN and U2AF1L4 can be necessary for regulation of T-cell activity.
Assuntos
Secretases da Proteína Precursora do Amiloide/genética , Regulação da Expressão Gênica , Proteínas de Membrana/genética , Proteínas Nucleares/genética , Regiões Promotoras Genéticas , Ribonucleoproteínas/genética , Secretases da Proteína Precursora do Amiloide/metabolismo , Linhagem Celular , Clonagem Molecular , Sequência Consenso , Humanos , Proteínas de Membrana/metabolismo , Proteínas Nucleares/química , Proteínas Nucleares/metabolismo , Motivos de Nucleotídeos , Especificidade de Órgãos/genética , Subunidades Proteicas/química , Subunidades Proteicas/genética , Subunidades Proteicas/metabolismo , Ribonucleoproteínas/química , Ribonucleoproteínas/metabolismo , Fator de Processamento U2AF , Transcrição GênicaRESUMO
Here we directly compared gene expression profiles in human esophageal squamous cell carcinomas and in human fetal esophagus development. We used the suppression subtractive hybridization technique to subtract cDNAs prepared from tumor and normal human esophageal samples. cDNA sequencing and reverse transcription polymerase chain reaction (RT-PCR) analysis of RNAs from human tumor and the normal esophagus revealed 10 differentially transcribed genes: CSTA, CRNN, CEACAM1, MAL, EMP1, ECRG2, and SPRR downregulated, and PLAUR, SFRP4, and secreted protein that is acidic and rich in cysteine upregulated in tumor tissue as compared with surrounding normal tissue. In turn, genes up- and downregulated in tumor tissue were down- and upregulated, respectively, during development from the fetal to adult esophagus. Thus, we demonstrated that, as reported for other tumors, gene transcriptional activation and/or suppression events in esophageal tumor progression were opposite to those observed during development from the fetal to adult esophagus. This tumor 'embryonization' supports the idea that stem or progenitor cells are implicated in esophageal cancer emergence.
