ArticleProceedings of the National Academy of Sciences of the United States of America2006
Identification of a Hoxc8-regulated transcriptional network in mouse embryo fibroblast cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Establishment of a xenograft model of endometriosis-associated fibrosis using human immortalized endometrial stromal cells overexpressing HOXC8.Scientific reports · 2026Article
- A prevalent disease-associated SNP in the humanNAR molecular medicine · 2026Article
- Tipifarnib Reduces Extracellular Vesicles and Protects From Heart Failure.Circulation research · 2024Article
- Viral remodeling of the 4D nucleome.Experimental & molecular medicine · 2024Review
- Association ofGenes · 2022Article
- Suv4-20h2 protects against influenza virus infection by suppression of chromatin loop formation.iScience · 2021Article
- Structural Equation Modeling and Whole-Genome Scans Uncover Chromosome Regions and Enriched Pathways for Carcass and Meat Quality in Beef.Frontiers in genetics · 2018Article
- Interleukin enhancer-binding factor 3 and HOXC8 co-activate cadherin 11 transcription to promote breast cancer cells proliferation and migration.Oncotarget · 2017Article
- HOXC8 regulates self-renewal, differentiation and transformation of breast cancer stem cells.Molecular cancer · 2017Article
- Genes Frequently Coexpressed with Hoxc8 Provide Insight into the Discovery of Target Genes.Molecules and cells · 2016Article
- Article
- HOXC8 promotes breast tumorigenesis by transcriptionally facilitating cadherin-11 expression.Oncotarget · 2014Article
- Deregulation of an imprinted gene network in prostate cancer.Epigenetics · 2014Article
- IGFBP3, a transcriptional target of homeobox D10, is correlated with the prognosis of gastric cancer.PloS one · 2013Article
- Homeobox D10 gene, a candidate tumor suppressor, is downregulated through promoter hypermethylation and associated with gastric carcinogenesis.Molecular medicine (Cambridge, Mass.) · 2012Article
- The crest phenotype in chicken is associated with ectopic expression of HOXC8 in cranial skin.PloS one · 2012Article
- HOXC8-Dependent Cadherin 11 Expression Facilitates Breast Cancer Cell Migration through Trio and Rac.Genes & cancer · 2011Article
- Hoxc8 downregulates Mgl1 tumor suppressor gene expression and reduces its concomitant function on cell adhesion.Molecules and cells · 2011Article
- Comparative transcriptome analyses indicate molecular homology of zebrafish swimbladder and mammalian lung.PloS one · 2011Article
- Comparing anterior and posterior Hox complex formation reveals guidelines for predicting cis-regulatory elements.Developmental biology · 2010Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The transcription factor, Hoxc8, is a member of the homeobox gene family that is vital for growth and differentiation. Previously, we identified 34 genes whose expression levels were changed at least 2-fold by forced expression of Hoxc8 in C57BL/6J mouse embryo fibroblast cells using a mouse 16,463-gene oligonucleotide microarray. In the present study, we used the combined power of microarray profiling, global Hoxc8 DNA-binding site analysis, and high-throughput chromatin immunoprecipitation assays to identify direct and biologically relevant targets of Hoxc8 in vivo. Here we show that 19 of the 34 responsive genes contain Hoxc8 consensus DNA-binding sequence(s) in their regulatory regions. Chromatin immunoprecipitation analysis indicated that Hoxc8-DNA interaction was detected in five of the 19 candidate genes. All of these five target genes have been implicated in oncogenesis, cell adhesion, proliferation, and apoptosis. Overall, the genes described here should aid in the understanding of global regulatory networks of Hox genes and to provide valuable insight into the molecular basis of Hoxc8 in development and carcinogenesis.
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