Duodenal mucosal risk markers in patients with familial adenomatous polyposis: effects of celecoxib/ursodeoxycholic acid co-treatment and comparison with patient controls

Heumen, Bjorn W H van; Roelofs, Hennie M.J.; Morsche, R.H.M. te; Nagengast, Fokko M.; Peters, Wilbert H.M.

doi:10.1186/1750-1172-8-181

Cited by 8 publications

(12 citation statements)

References 40 publications

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“…Between familial adenomatous polyposis (FAP) and non-FAP groups, over-expression of CEMIP had no clear relationship. This result further indicated the high expression of CEMIP might particularly appear in the proliferation and canceration of colorectal and gastric cancer cells 15 .…”

Section: The Relationship Between Non-tumor Disease and Cemipmentioning

confidence: 69%

“…A status of nuclear confinement for CEMIP illustrated a relatively safe situation for cancer patient. It also might be the evidence for early medical intervention or diagnostic indicator when patients suffered aggressive tumor 14 , 15 . Though the expression of CEMIP, placed in the nucleus, was discovered in colon adenomas regardless the UICC stage, the localization of CEMIP in the nucleus and its over-expression might be linked to the presence of β-catenin in nucleus 3 .…”

Section: Introductionmentioning

confidence: 99%

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Central Role of CEMIP in Tumorigenesis and Its Potential as Therapeutic Target

Li¹,

Yan²,

Manoj³

et al. 2017

J. Cancer

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CEMIP (KIAA1199) was identified as migratory indicator protein which had been crudely studied in the last decade. Firstly its mutation site was reported to cause hearing loss due to the folding change of protein structure, meanwhile the over-expression of CEMIP referred to dreadful invasion and uncontrolled proliferation of tumor with distant metastasis, dedifferentiation, and limited survival opportunity of patients. Especially, over-expressed CEMIP also protected malignant tumor from strict microenvironment in hypoxia, low glucose and cracked barrier, leading to enhanced adaptability of tumor by stimulating the Wnt, EGFR, FGFR pathway. Here, we intend to elaborate the clinical function and dysregulation of CEMIP under the tumorous circumstance since CEMIP plays an important role in cytokine pathway and its over-expression in tumors provide a novel target for individual therapy. Targeting CEMIP would thereby dysregulate the cytokine pathway which would in turn, decide the growth and death of the vicious tumour cells.

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Section: The Relationship Between Non-tumor Disease and Cemipmentioning

confidence: 69%

Section: Introductionmentioning

confidence: 99%

Central Role of CEMIP in Tumorigenesis and Its Potential as Therapeutic Target

Li¹,

Yan²,

Manoj³

et al. 2017

J. Cancer

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“…The wide variety of beneficial effects of UDCA may be related to its multiple mechanisms of action. UDCA has been shown to interact with cyclooxygenase 2 (COX-2), epidermal growth factor receptor (EGFR), and their downstream mediators in some hepatocyte and enterocyte signaling pathways (10,25,28,42,46,55,56). In addition, COX-2 and EGFR seem to play a role in enterocyte migration (19,26,39,41,52).…”

Section: Introductionmentioning

confidence: 99%

Ursodeoxycholic acid protects against intestinal barrier breakdown by promoting enterocyte migration via EGFR- and COX-2-dependent mechanisms

Golden

Escobar

Nguyen

et al. 2018

American Journal of Physiology-Gastrointestinal and Liver Physi

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The intestinal barrier is often disrupted in disease states, and intestinal barrier failure leads to sepsis. Ursodeoxycholic acid (UDCA) is a bile acid that may protect the intestinal barrier. We hypothesized that UDCA would protect the intestinal epithelium in injury models. To test this hypothesis, we utilized an in vitro wound-healing assay and a mouse model of intestinal barrier injury. We found that UDCA stimulates intestinal epithelial cell migration in vitro, and this migration was blocked by inhibition of cyclooxygenase 2 (COX-2), epidermal growth factor receptor (EGFR), or ERK. Furthermore, UDCA stimulated both COX-2 induction and EGFR phosphorylation. In vivo UDCA protected the intestinal barrier from LPS-induced injury as measured by FITC dextran leakage into the serum. Using 5-bromo-2'-deoxyuridine and 5-ethynyl-2'-deoxyuridine injections, we found that UDCA stimulated intestinal epithelial cell migration in these animals. These effects were blocked with either administration of Rofecoxib, a COX-2 inhibitor, or in EGFR-dominant negative Velvet mice, wherein UDCA had no effect on LPS-induced injury. Finally, we found increased COX-2 and phosphorylated ERK levels in LPS animals also treated with UDCA. Taken together, these data suggest that UDCA can stimulate intestinal epithelial cell migration and protect against acute intestinal injury via an EGFR- and COX-2-dependent mechanism. UDCA may be an effective treatment to prevent the early onset of gut-origin sepsis. NEW & NOTEWORTHY In this study, we show that the secondary bile acid ursodeoxycholic acid stimulates intestinal epithelial cell migration after cellular injury and also protects the intestinal barrier in an acute rodent injury model, neither of which has been previously reported. These effects are dependent on epidermal growth factor receptor activation and downstream cyclooxygenase 2 upregulation in the small intestine. This provides a potential treatment for acute, gut-origin sepsis as seen in diseases such as necrotizing enterocolitis.

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“…Using this technology, researchers have found that the CNV of a specific region associated with pancreatic cancer risk is likely due to an effect on the long-term regulation of CDKN2B [19]. Moreover, the QuantiGene assay may be more significant in cancer research owing to its high accuracy and convenience for use with many types of samples, including blood, tissues, and, most importantly, formalin-fixed paraffin-embedded (FFPE) slides, which are easily accessed in a clinical setting [20].…”

Section: Introductionmentioning

confidence: 99%