COX-2 mRNA Expression is Significantly Increased in Acid-exposed Compared to Nonexposed Squamous Epithelium in Gastroesophageal Reflux Disease

Lurje, Georg; Vallböhmer, Daniel; P, Collet; Hao, Xi Shan; Baldus, Stephan; Brabender, Jan; Metzger, Ralf; Heitmann, Michaela; Neiss, Susanne; Drebber, U.; Hölscher, A. H.; Schneider, Paul M.

doi:10.1007/s11605-007-0210-3

Cited by 12 publications

(4 citation statements)

References 20 publications

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“…COX‐2 protein and mRNA expression is induced by bile acids and has also been found to be induced in some malignant processes 20,21 . COX‐2 expression can be induced in cultured human pharyngeal cells by bile, acid or both, implying that LPR may have a role in malignant transformation in the upper aerodigestive tract 18 …”

Section: Discussionmentioning

confidence: 99%

Reflux changes in adenoidal hyperplasia: a controlled prospective study to investigate its aetiology

Harris

Hussey

Watson

et al. 2009

Clinical Otolaryngology

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Our results suggest that the biochemical changes seen in adenoid hypertrophy are different to those seen in reflux-affected tissues. The decreased COX-2 and MUC5AC expression may be due to squamous metaplasia and other inflammatory changes associated with adenoid hypertrophy. Our findings infer there is little evidence of reflux being a major contributory factor in the pathophysiology of adenoidal hypertrophy.

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Section: Discussionmentioning

confidence: 99%

Reflux changes in adenoidal hyperplasia: a controlled prospective study to investigate its aetiology

Harris

Hussey

Watson

et al. 2009

Clinical Otolaryngology

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“…Earlier, studies have reported that COX-2 expression is unregulated in precancerous lesions and preinvasive carcinoma and positively correlates with tumor invasion and lymphatic metastasis (Lurje et al, 2007;Strazisar et al, 2009). Therefore, increasing expression of COX-2 might occur in the early stages of the tumor and the detection of COX-2 level is helpful for early diagnosis of CRC.…”

Section: Introductionmentioning

confidence: 99%

Over-Expression of Cyclooxygenase-2 in Colorectal Cancer Patients

Negi

Rana

Gupta

et al. 2019

Asian Pac J Cancer Prev

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100,000, respectively. Whereas, AAR for colon cancer in women is 3.9 per 100,000. Colon cancer ranks 8th and rectal cancer ranks 9th among men in India (NCRP, 2013).The development of colorectal cancer is a highly complex and multistep process and is linked to mutations that may occur in the oncogenes K-ras and APC or in the tumor suppressor gene p53, thereby causing uncontrolled proliferation of cells. Cell proliferation is pivotal in tumorigenesis and Cyclooxygenases (COXs) are important regulatory

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“…SOX9 is also essential in the development of embryonic columnar-lined esophagus but is switched off in postnatal life and is reexpressed again in BM (14,28,49). Expression of cyclooxygenase-2 (COX-2) is upregulated and plays has a key role in the development of BM, possibly by disrupting key signaling pathways that maintain homeostasis in the NES epithelium (22).…”

mentioning

confidence: 99%

Barrett’s metaplasia develops from cellular reprograming of esophageal squamous epithelium due to gastroesophageal reflux

Minacapelli

Bajpai

Geng

et al. 2017

American Journal of Physiology-Gastrointestinal and Liver Physi

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Gastroesophageal reflux disease (GERD) clinically predisposes to columnar Barrett's metaplasia (BM) in the distal esophagus. We demonstrate evidence supporting the cellular origin of BM from reprograming or transcommitment of resident normal esophageal squamous (NES) epithelial cells in response to acid and bile (A + B) exposure using an in vitro cell culture model. The hTERT-immortalized NES cell line NES-B10T was exposed 5 min/day to an A + B mixture for 30 wk. Morphological changes, mRNA, and protein expression levels for the inflammatory marker cyclooxygenase-2; the lineage-determining transcription factors TAp63 (squamous), CDX2, and SOX9 (both columnar); and the columnar lineage markers Villin, Muc-2, CK8, and mAb Das-1 (incomplete phenotype of intestinal metaplasia) were assessed every 10 wk. Markers of columnar lineage and inflammation increased progressively, while squamous lineage-determining transcriptional factors were significantly decreased both at the mRNA and/or protein level in the NES-B10T cells at/after A + B treatment for 30 wk. Distinct modifications in morphological features were only observed at/after 30 wk of A + B exposure. These changes acquired by the NES-B10T 30-wk cells were retained even after cessation of A + B exposure for at least 3 wk. This study provides evidence that chronic exposure to the physiological components of gastric refluxate leads to repression of the discernable squamous transcriptional factors and activation of latent columnar transcriptional factors. This reflects the alteration in lineage commitment of the precursor-like biphenotypic, NES-B10T cells in response to A + B exposure as the possible origin of BM from the resident NES cells. This study provides evidence of the origins of Barrett's metaplasia from lineage transcommitment of resident esophageal cells after chronic exposure to gastroesophageal refluxate. The preterminal progenitor-like squamous cells alter their differentiation and develop biphenotypic characteristics, expressing markers of incomplete-type columnar metaplasia. Development of these biphenotypic precursors in vitro is a unique model to study pathogenesis of Barrett's metaplasia and esophageal adenocarcinoma.

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COX-2 mRNA Expression is Significantly Increased in Acid-exposed Compared to Nonexposed Squamous Epithelium in Gastroesophageal Reflux Disease

Cited by 12 publications

References 20 publications

Reflux changes in adenoidal hyperplasia: a controlled prospective study to investigate its aetiology

Reflux changes in adenoidal hyperplasia: a controlled prospective study to investigate its aetiology

Over-Expression of Cyclooxygenase-2 in Colorectal Cancer Patients

Barrett’s metaplasia develops from cellular reprograming of esophageal squamous epithelium due to gastroesophageal reflux

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