Cdx genes, inflammation and the pathogenesis of Barrett's metaplasia

Colleypriest, Benjamin J.; Palmer, Rebecca; Ward, Stephen G.; Tosh, David

doi:10.1016/j.molmed.2009.05.001

Cited by 26 publications

(21 citation statements)

References 93 publications

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“…However, CDX2 is reported to be decreased in the presence of dysplasia (5). Colleypriest et al has found CDX2 mRNA in 1/3 of the BE patients in the SE, a result showing that CDX2 expression preceeds the phenotypic changes (7).…”

Section: Introductionmentioning

confidence: 98%

CDX2, COX2 and MUC2 Expressions in Barrett's Esophagus: Can They Be Useful in Determination of the Dysplasia?

Iç¹,

Başsüllü²,

Uraz³

et al. 2012

TJPATH

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Section: Introductionmentioning

confidence: 98%

CDX2, COX2 and MUC2 Expressions in Barrett's Esophagus: Can They Be Useful in Determination of the Dysplasia?

Iç¹,

Başsüllü²,

Uraz³

et al. 2012

TJPATH

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“…Induction of caudal type homeobox 2 (CDX2) and cyclooxygenase 2 (COX-2) expression is a crucial molecular event in the development of BE and EAC [3,4]. The transcription factor CDX2 plays important roles in the development and maintenance of normal intestinal tissue, and its aberrant expression contributes to the pathogenesis of BE [5,6].…”

Section: Introductionmentioning

confidence: 99%

Guggulsterone, a Plant-Derived Inhibitor of NF-TB, Suppresses CDX2 and COX-2 Expression and Reduces the Viability of Esophageal Adenocarcinoma Cells

Yamada

Osawa²,

Ikuma

et al. 2014

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Background/Aims: Induction by bile acid of caudal type homeobox 2 (CDX2) and cyclooxygenase-2 (COX-2) expression via nuclear factor-TB (NF-TB) activation is a critical event in the development of Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). Guggulsterone (GS) is a plant sterol that inhibits NF-TB activity. Here, we evaluated whether GS has either or both chemopreventive or therapeutic effects against EAC. Methods: Two EAC cells lines were treated with deoxycholic acid (DCA) in the presence of GS or vehicle. The levels of transcription and translation of ITBE, CDX2, and COX-2 were determined. Prostaglandin E₂ (PGE₂) levels, cell viability, and cell cycle distribution were assessed as well. Results: GS inhibited DCA-induced ITBE phosphorylation. GS and the NF-TB inhibitor BAY11-7085 suppressed DCA-induced CDX2 and COX-2 expression in EAC cells. GS also suppressed basal transcription levels of CDX2 and COX-2 and reduced constitutive synthesis of COX-2 and PGE₂. Further, GS reduced the viability of EAC cells, increased their numbers in the apoptotic sub-G1 fraction. Conclusion: GS suppressed DCA-induced and NF-TB-dependent activation of CDX2 and COX-2 expression. Further, GS also reduced the viability of EAC cells. GS may serve as candidate for preventing and treating EAC and BE. i 2014 S. Karger AG, Basel

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“…[1][2][3] As a Caudal-related homeobox gene that is essential for skeletal and intestinal development, Cdx2 has been suggested to play an important role in IM (e.g., esophagus, stomach, and bile duct) and cancers (e.g., colon cancer, leukemia). 4,5 Squamous epithelial cells of normal human esophagus do not express Cdx2, while submucosal glands weakly express Cdx2 protein in the cytoplasm.…”

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confidence: 99%

Transgenic Overexpression of cdx1b Induces Metaplastic Changes of Gene Expression in Zebrafish Esophageal Squamous Epithelium

Chen

Liu³

et al. 2013

Zebrafish

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Cdx2 has been suggested to play an important role in Barrett's esophagus or intestinal metaplasia (IM) in the esophagus. To investigate whether transgenic overexpression of cdx1b, the functional equivalent of mammalian Cdx2 in zebrafish, may lead to IM of zebrafish esophageal squamous epithelium, a transgenic zebrafish system was developed by expressing cdx1b gene under the control of zebrafish keratin 5 promoter (krt5p). Gene expression in the esophageal squamous epithelium of wild-type and transgenic zebrafish was analyzed by Affymetrix microarray and confirmed by in situ hybridization. Morphology, mucin expression, cell proliferation, and apoptosis were analyzed by hematoxylin & eosin (HE) staining, Periodic acid Schiff (PAS) Alcian blue staining, proliferating cell nuclear antigen (PCNA) immunohistochemical staining, and TUNEL assay as well. cdx1b was found to be overexpressed in the nuclei of esophageal squamous epithelial cells of the transgenic zebrafish. Ectopic expression of cdx1b disturbed the development of this epithelium in larval zebrafish and induced metaplastic changes in gene expression in the esophageal squamous epithelial cells of adult zebrafish, that is, up-regulation of intestinal differentiation markers and down-regulation of squamous differentiation markers. However, cdx1b failed to induce histological IM, or to modulate cell proliferation and apoptosis in the squamous epithelium of adult transgenic zebrafish.

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Cdx genes, inflammation and the pathogenesis of Barrett's metaplasia

Cited by 26 publications

References 93 publications

CDX2, COX2 and MUC2 Expressions in Barrett's Esophagus: Can They Be Useful in Determination of the Dysplasia?

CDX2, COX2 and MUC2 Expressions in Barrett's Esophagus: Can They Be Useful in Determination of the Dysplasia?

Guggulsterone, a Plant-Derived Inhibitor of NF-TB, Suppresses CDX2 and COX-2 Expression and Reduces the Viability of Esophageal Adenocarcinoma Cells

Transgenic Overexpression of cdx1b Induces Metaplastic Changes of Gene Expression in Zebrafish Esophageal Squamous Epithelium

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