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The ACVR1 gene encodes a type I receptor for bone morphogenetic proteins (BMPs). Mutations in the ACVR1 gene are associated with Fibrodysplasia Ossificans Progressiva (FOP), a rare and extremely disabling disorder characterized by congenital malformation of the great toes and progressive heterotopic endochondral ossification in muscles and other non-skeletal tissues. Several aspects of FOP pathophysiology are still poorly understood, including mechanisms regulating ACVR1 expression. This work aimed to identify regulatory elements that control ACVR1 gene transcription.
Methods and results
We first characterized the structure and composition of human ACVR1 gene transcripts by identifying the transcription start site, and then characterized a 2.9 kb upstream region. This region showed strong activating activity when tested by reporter gene assays in transfected cells. We identified specific elements within the 2.9 kb region that are important for transcription factor binding using deletion constructs, co-transfection experiments with plasmids expressing selected transcription factors, site-directed mutagenesis of consensus binding-site sequences, and by protein/DNA binding assays. We also characterized a GC-rich minimal promoter region containing binding sites for the Sp1 transcription factor.
Our results showed that several transcription factors such as Egr-1, Egr-2, ZBTB7A/LRF, and Hey1, regulate the ACVR1 promoter by binding to the -762/-308 region, which is essential to confer maximal transcriptional activity. The Sp1 transcription factor acts at the most proximal promoter segment upstream of the transcription start site. We observed significant differences in different cell types suggesting tissue specificity of transcriptional regulation. These findings provide novel insights into the molecular mechanisms that regulate expression of the ACVR1 gene and that could be targets of new strategies for future therapeutic treatments.
ACVR1, Fibrodysplasia ossificans progressiva (FOP), ACVR1 promoter, Transcriptional regulation, BMP signaling Go to: Background
Identification and characterization of regulatory elements in the promoter of ACVR1, the gene mutated in Fibrodysplasia Ossificans Progressiva
Francesca Giacopelli,1 Serena Cappato,1 Laura Tonachini,1 Marzia Mura,1 Simona Di Lascio,2 Diego Fornasari,2,3 Roberto Ravazzolo,1,4 and Renata Bocciardicorresponding author1,4
Food allergy poses a significant clinical and public health burden affecting 2-10% of infants. Using integrated DNA methylation and transcriptomic profiling, we found that polyclonal activation of naive CD4+ T cells through the T cell receptor results in poorer lymphoproliferative responses in children with immunoglobulin E (IgE)-mediated food allergy. Reduced expression of cell cycle-related targets of the E2F and MYC transcription factor networks, and remodeling of DNA methylation at metabolic (RPTOR, PIK3D, MAPK1, FOXO1) and inflammatory genes (IL1R, IL18RAP, CD82) underpins this suboptimal response. Infants who fail to resolve food allergy in later childhood exhibit cumulative increases in epigenetic disruption at T cell activation genes and poorer lymphoproliferative responses compared to children who resolved food allergy. Our data indicate epigenetic dysregulation in the early stages of signal transduction through the T cell receptor complex, and likely reflects pathways modified by gene-environment interactions in food allergy.
Epigenetic dysregulation of naive CD4+ T-cell activation genes in childhood food allergy
David Martino,1,2 Melanie Neeland,1 Thanh Dang,1 Joanna Cobb,1 Justine Ellis,1 Alice Barnett,1 Mimi Tang,1 Peter Vuillermin,1,3,4 Katrina Allen,corresponding author1 and Richard Saffery1
Accumulated evidence suggests that dysregulated expression of long non-coding RNAs (lncRNAs) may play a critical role in tumorigenesis and prognosis of cancer, indicating the potential utility of lncRNAs as cancer prognostic or diagnostic markers. However, the power of lncRNA signatures in predicting the survival of patients with non-small cell lung cancer (NSCLC) has not yet been investigated.
We performed an array-based transcriptional analysis of lncRNAs in large patient cohorts with NSCLC by repurposing microarray probes from the gene expression omnibus database. A risk score model was constructed based on the expression data of these eight lncRNAs in the training dataset of NSCLC patients and was subsequently validated in other two independent NSCLC datasets. The biological implications of prognostic lncRNAs were also analyzed using the functional enrichment analysis.
An expression pattern of eight lncRNAs was found to be significantly associated with overall survival (OS) of NSCLC patients in the training dataset. With the eight-lncRNA signature, patients of the training dataset could be classified into high- and low-risk groups with significantly different OS (median survival 1.67 vs. 6.06 years, log-rank test p = 4.33E−09). The prognostic power of eight-lncRNA signature was further validated in other two non-overlapping independent NSCLC cohorts, demonstrating good reproducibility and robustness of this eight-lncRNA signature in predicting OS of NSCLC patients. Multivariate regression and stratified analysis suggested that the prognostic power of the eight-lncRNA signature was independent of clinical and pathological factors. Functional enrichment analyses revealed potential functional roles of the eight prognostic lncRNAs in tumorigenesis.
These findings indicate that the eight-lncRNA signature may be an effective independent prognostic molecular biomarker in the prediction of NSCLC patient survival.
Electronic supplementary material
The online version of this article (doi:10.1186/s12967-015-0556-3) contains supplementary material, which is available to authorized users.
Long non-coding RNA, Non-small cell lung cancer, Overall survival, Signature
A potential signature of eight long non-coding RNAs predicts survival in patients with non-small cell lung cancer
Meng Zhou,# Maoni Guo,# Dongfeng He,# Xiaojun Wang, Yinqiu Cui, Haixiu Yang, Dapeng Hao,corresponding author and Jie Suncorresponding author