HDAC7, is involved in tumor initiation and development. HDAC7 might be a critical player in tumor angiogenesis which is essential for solid tumor growth and metastasis. HDAC7 is necessary for human umbilical vein endothelial cells grown on Matrigel to form primitive vascular-like structures. Its silencing changes cell morphology and decreases endothelial cell migration, partially through an upregulation of platelet-derived growth factor and its receptor. HDAC7 represses the expression of matrix metalloproteinase (MMP) 10 in the vascular endothelium during early embryogenesis, and the absence of HDAC7 gene in mice results in embryonic lethality due to the rupture of blood vessels caused by MMP 10 overexpression. HDAC7 also binds and increases the transcriptional activity of hypoxia-inducible factor 1α (HIF-1α), a master regulator of angiogenesis in hypoxia. Besides regulating angiogenesis, HDAC7 also functions in apoptosis regulation. It is reported that mitochondrial and nuclear HDAC7 would redistribute to the cytoplasm upon induction of apoptotic cascade. The phosphorylation status of HDAC7 is modulated by protein phosphatase 2A and protein kinase D and related with its subcellular localization and T cell apoptosis.
Zhu C, et al. The role of histone deacetylase 7 (HDAC7) in cancer cell proliferation: regulation on c-Myc[J]. Journal of molecular medicine, 2011, 89(3): 279-289.