Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0154059 (Esophagus)
 2,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate cyclooxygenase-2 (COX-2) mRNA expression in human esophageal squamous cell carcinoma and the effect of a non-steroidal anti-inflammatory drug (NSAID) on it, in order to explore the mechanism of COX-2 in esophageal squamous cell carcinoma (ESCC) carcinogenesis and the ability of NSAID to prevent or treat ESCC. Frozen specimens of human ESCC and adjacent normal esophageal squamous epithelium pairs (n = 22) were examined for COX-2 mRNA expression by reverse-transcription polymerase chain reaction (RT-PCR). After incubation with aspirin (a non-selective COX inhibitor) or Nimesulide (a selective COX-2 inhibitor), the proliferation status of two human esophageal squamous cancer cell lines, EC-9706 and EC-109, was quantified by 3-(4,5-dimethyl-thiazol-2yl)-2,5-diphenyltetrazolium bromide assay. The expression of COX-2 mRNA in these cells was detected by RT-PCR. COX-2 mRNA was expressed in 12 of 22 (54.5%) ESCC tissue samples, but it was undetectable in all the specimens of adjacent normal esophageal squamous epithelium COX-2 mRNA expression. Both aspirin (5-20 mmol/L) and Nimesulide (0.1-0.8 mmol/L) inhibited EC-9706 cell line proliferation and suppressed its COX-2 mRNA expression dose-dependently. However, only aspirin (5-20 mmol/L) could inhibit proliferation in the EC-109 cell line and suppress COX-2 mRNA expression. Nimesulide (0.1-0.8 mmol/L) could neither inhibit EC-109 cell growth nor suppress COX-2 mRNA expression. COX-2 mRNA expression is a frequent phenomenon in human ESCC tissue samples and plays an important role in the carcinogenesis of ESCC. NSAID may be useful in the chemoprevention and therapy of human ESCC and its effects are likely to be mediated by modulating COX-2 activity.
Dis Esophagus 2008
PMID:COX-2 mRNA expression in esophageal squamous cell carcinoma (ESCC) and effect by NSAID. 1819 33

The objective of this study is to investigate the effects of aspirin and nimesulide on cell proliferation, apoptosis and its potential mechanisms in EC9706 and EC109 esophageal squamous carcinoma cells. EC9706 and EC109 cells were incubated with varying concentrations of aspirin and nimesulide, and the effects on cell proliferation and apoptosis were monitored by 3-(4,5-dimethyl-thiazol-2yl)-2,5-diphenyltetrazolium bromide and flow cytometry. Reverse transcription-polymerase chain reaction and Western blot assays were used to investigate expression of Bcl-2 and Bax. Prostaglandin E2 production was measured by enzyme linked immunosorbent assay. Pretreatment with aspirin and nimesulide inhibited EC9706 and EC109 cell growth in a time and dose-dependent manner, accompanied with a decrease of prostaglandin E2 production. In EC9706 cells, the mechanism of aspirin and nimesulide induced growth inhibition was a consequence of cell cycle arrest at the G(0)/G(1) check point. In EC109 cells, growth arrest was by induction of apoptosis, associated with downregulation of Bcl-2, but not Bax. In conclusion, aspirin and nimesulide could inhibit cell proliferation and induce apoptosis in esophageal squamous carcinoma cells. Cyclooxygenase-2 inhibitor may be a promising therapeutic agent for human esophageal squamous cell carcinoma.
Dis Esophagus 2009
PMID:Effects of cyclooxygenase-2 non-selective and selective inhibitors on proliferation inhibition and apoptosis induction of esophageal squamous carcinoma cells. 1856 72

The relationship between smoking and esophageal squamous cell carcinoma (ESCC) has been confirmed by epidemiology. Cyclin D(1) plays a critical role in regulating the cell cycle; it is an important regulator of cell cycle and can function as a transcriptional co-regulator. The importance of cyclin D(1) makes it an attractive target for anticancer therapy. Human ESCC cell line EC109 was cultured with aspirin and cigarette smoke extract (CSE) at different concentrations for 48 h. Cell growth was tested with 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide reduction assay; cyclin D(1) mRNA level was detected by reverse transcription-polymerase chain reaction assays; protein level of cyclin D(1) was detected by Western blot; the cell cycle change was monitored by flow cytometry detection assays. CSE stimulated cell proliferation, increased the protein level of cyclin D(1) in a dose-dependent manner (P < 0.01), and decreased the proportion of G(0)/G(1) phase cell of cell cycle. However, aspirin can inhibit the cell growth and suppress the protein level of cyclin D(1) after CSE affected the EC109 cell line in a dose-dependent manner (P < 0.01). Meanwhile, aspirin increased the proportion of G(0)/G(1) phase cell, while that of S and G(2)/M phases decreased. Aspirin can inhibit the cell growth and suppress the protein level of cyclin D(1) after CSE affected EC109 cell line. The probable mechanism is through decreasing the expression of cyclin D(1), thus stopping the transition of cell cycle from G(0)/G(1) to S phase.
Dis Esophagus 2009
PMID:Influence of aspirin and cigarette smoke extract on the expression of cyclin D1 and effects of cell cycle in esophageal squamous cell carcinoma cell line. 1920 49