2004
DOI: 10.1038/sj.onc.1207160
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Identification of IGFBP-6 as a significantly downregulated gene by β-catenin in desmoid tumors

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Cited by 39 publications
(39 citation statements)
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References 24 publications
(25 reference statements)
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“…In NCI-H1299 cells, TCF activity is induced by introducing b-catenin cDNA (Usami et al, 2003). The IGFBP-6 promoter has two copies of TCFbinding motifs, and b-catenin suppresses the expression of IGFBP-6 through these motifs (Denys et al, 2004). These results suggest that, in NCI-H1299 cells, b-catenin may antagonize the tumor suppressor activity of SEMA3B by inhibiting the expression of IGFBP-6.…”
Section: Identification Of Igfbp-6mentioning
confidence: 71%
“…In NCI-H1299 cells, TCF activity is induced by introducing b-catenin cDNA (Usami et al, 2003). The IGFBP-6 promoter has two copies of TCFbinding motifs, and b-catenin suppresses the expression of IGFBP-6 through these motifs (Denys et al, 2004). These results suggest that, in NCI-H1299 cells, b-catenin may antagonize the tumor suppressor activity of SEMA3B by inhibiting the expression of IGFBP-6.…”
Section: Identification Of Igfbp-6mentioning
confidence: 71%
“…Increased β-catenin levels have been causatively linked to increased broblast proliferation in aggressive bromatosis (desmoid tumor) [27,28] and hypertrophic scar formation [22]. As these conditions share many molecular similarities with FSS and DD [18,29], β-catenin is likely to play analogous broproliferative roles in these diseases. Western immunoblotting also revealed the presence of multiple molecular weight forms of β-catenin in FSS tissues, correlating with similar observations in DD tissues [17].…”
mentioning
confidence: 99%
“…14 -16 Further findings suggest that insulin-like growth factor binding protein 6 (IGFBP-6) is downregulated directly by the ␤-catenin/TCF complex in adult AF and implies a role for the IGF axis in the proliferation of AF. 30 A recent review reported a high prevalence of desmoid tumor in 126 of 880 adult patients with FAP (14.3%) who had proven AF gene mutation, 19 and an extremely high prevalence (38%) was reported for patients with Gardner syndrome. 20 In pediatric AF studies, no patient with a history of familial AF or FAP and only two patients with Gardner syndrome were reported.…”
Section: Discussionmentioning
confidence: 99%