Effect of Disrupted SOX18 Transcription Factor Function on Tumor Growth, Vascularization, and Endothelial Development

Abstract

SOX18 is a potential target for antiangiogenic therapy of human cancers.

The lymphangiogenic factor SOX 18: A key indicator to stage gastric tumor progression

“…[19][20][21][22][23][24][25][26][27][28][29][30] In fact, few studies have revealed the significance of SOX group F gene expression in human cancer, although cell line-based studies have demonstrated that both SOX 18 and SOX 7 were highly expressed in several strains of gastric, pancreatic and esophageal cancer cell lines. 22,32 In the present study, SOX group F gene expression determined by RT-PCT was increased in gastric cancer tissues than in normal gastric tissues obtained from the same individuals.…”

“…22 SOX 18 expression is also reactivated during adult neovascularization associated with wound healing and tumorigenesis. 23,24 Thus, interfering with SOX 18 function, both blood vessel formation and subsequent tumor growth …”

“…22 SOX 18 expression is also reactivated during adult neovascularization associated with wound healing and tumorigenesis. 23,24 Thus, interfering with SOX 18 function, both blood vessel formation and subsequent tumor growth are inhibited and this process is responsible for the lymphatic defect in hypotrichosis-lymphoedema-telangiectasia. [25][26][27][28] The SOX 7 and SOX 17 genes are also known to have compensatory roles during angiogenesis and lymphangiogenesis.…”

Sox7 in vascular development: review, insights and potential mechanisms

“…SoxF subgroup members in Drosophila and vertebrates also share highly conserved intronic positions, which represent ancient introns present before vertebrate lineage divergence (Bowles et al, 2000;Kanai et al, 1996;Taniguchi et al, 1999). Expression of mouse Sox18 across embryonic and adult tissue Northern blot analyses occurs in a very similar pattern to that of Sox7; furthermore, Sox7, Sox17, and Sox18 each colocalize to the developing mouse embryonic vasculature (Takash et al, 2001;Young et al, 2006). Functionally, Sox7 and Sox17 can also activate Sox18 targets and modify the Sox18 mutant mouse phenotype (Hosking et al, 2009).…”

“…At 9.5 dpc and 11.5 dpc, Sox7 is expressed in the intersomitic vessels and endothelial cells lining the posterior dorsal aorta and in the anterior neural medial axial artery (Young et al, 2006;Takash et al, 2001). At 9.5 dpc, Sox7 expression is also found in small branching vessels, throughout the embryonic vasculature, a In some tumors, such as colorectal and prostate, Sox7 down-regulation was partly due to hypermethylation at its promoter (Guo et al, 2008;Zhang et al, 2009). and in the atria (Takash et al, 2001).…”