The dual roles of homeobox genes in vascularization and wound healing

Homeobox genes represent a family of highly conserved transcription factors originally discovered to regulate organ patterning during development. More recently, several homeobox genes were shown to affect processes in adult tissue, including angiogenesis and wound healing. Whereas a subset of membe...

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Bibliographic Details
Published in:Cell adhesion & migration 2012-11, Vol.6 (6), p.457-470
Main Authors: Kachgal, Suraj, Mace, Kimberly A., Boudreau, Nancy J.
Format: Article
Language:English
Subjects:
angiogenesis
Animals
Cell Differentiation
Cell Survival
Chemokine CCL2 - genetics
Chemokine CCL2 - metabolism
Disease Progression
endothelial cells
Endothelial Cells - metabolism
Gene Expression Regulation, Neoplastic
Genes, Homeobox
Homeodomain Proteins - genetics
Homeodomain Proteins - metabolism
Hox genes
Humans
inflammation
Neoplasm Metastasis
Neoplasms - genetics
Neoplasms - metabolism
Neoplasms - pathology
Neovascularization, Pathologic - genetics
Neovascularization, Pathologic - metabolism
Neovascularization, Pathologic - pathology
Review
Transcriptional Activation
tumor vascularization
Wound Healing
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Summary:Homeobox genes represent a family of highly conserved transcription factors originally discovered to regulate organ patterning during development. More recently, several homeobox genes were shown to affect processes in adult tissue, including angiogenesis and wound healing. Whereas a subset of members of the Hox-family of homeobox genes activate growth and migration to promote angiogenesis or wound healing, other Hox genes function to restore or maintain quiescent, differentiated tissue function. Pathological tissue remodeling is linked to differential expression of activating or stabilizing Hox genes and dysregulation of Hox expression can contribute to disease progression. Studies aimed at understanding the role and regulation of Hox genes have provided insight into how these potent morphoregulatory genes can be applied to enhance tissue engineering or limit cancer progression.
ISSN:1933-6918
1933-6926
DOI:10.4161/cam.22164