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Neoadjuvant selective COX-2 inhibition down-regulates important oncogenic pathways in patients with esophageal
Jurriaan B Tuynman1, Christianne J Buskens, Kristel Kemper
1Departments of Surgery, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. J.B.Tuynman@amc.uva.nl
Objectives:
To evaluate the effects of neoadjuvant therapy with the selective cyclooxygenase-2 (COX-2) inhibitor celecoxib in vitro and in patients with esophageal adenocarcinoma on COX-2 and MET expression.
Summary Background Data:
High COX-2 and/or MET expression levels are negative prognostic factors for adenocarcinoma of the esophagus. Nonsteroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors exert anticancer mechanisms as is evident from epidemiologic studies and from experimental models for esophageal cancer. The mechanisms and the significance of these findings in patients with adenocarcinoma of the esophagus are unknown.
Methods:
Esophageal adenocarcinoma cell lines were used to asses the effects in vitro. To study the clinical effects 12 patients with esophageal adenocarcinoma were included for neoadjuvant treatment (4 weeks) with celecoxib at 400 mg twice daily. Fifteen patients not receiving NSAIDs or celecoxib were included as a control. Effects were evaluated using the MTT-cell viability test, Western blot analysis, immunohistochemistry, and RT-PCR.
Results:
In vitro celecoxib administration resulted in decreased cell viability, increased apoptosis, and decreased COX-2 and MET expression levels. In patients, neoadjuvant treatment with celecoxib significantly down-regulated COX-2 and MET expression in the tumor when compared with the nontreated control group and when compared with pretreatment measurements.
Conclusions:
This is the first study to show in vitro and in patients with esophageal adenocarcinoma that selective COX-2 inhibition down-regulates COX-2 and MET expression, both important proteins involved in cancer progression and dissemination. Therefore, (neo)adjuvant therapy with celecoxib might have clinical potential for patients with esophageal adenocarcinoma.
Insights
Celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, reduced esophageal adenocarcinoma cell viability and down-regulated COX-2 and MET expression in vitro and in patients. This suggests potential for celecoxib in treating esophageal adenocarcinoma.
Area of Science:
- Oncology
- Gastroenterology
- Pharmacology
Background:
- High expression of cyclooxygenase-2 (COX-2) and MET are negative prognostic factors in esophageal adenocarcinoma.
- Nonsteroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 inhibitors show anticancer effects in esophageal cancer models.
- The clinical significance of these effects in esophageal adenocarcinoma patients remains unclear.
Purpose of the Study:
- To evaluate the in vitro and clinical effects of neoadjuvant celecoxib on COX-2 and MET expression in esophageal adenocarcinoma.
- To assess the impact of selective COX-2 inhibition on cancer progression markers.
Main Methods:
- In vitro studies used esophageal adenocarcinoma cell lines with MTT-cell viability assays, Western blot, immunohistochemistry, and RT-PCR.
- A clinical trial involved 12 patients with esophageal adenocarcinoma receiving neoadjuvant celecoxib (400 mg twice daily for 4 weeks).
- A control group of 15 patients not receiving NSAIDs or celecoxib was included for comparison.
Main Results:
- In vitro, celecoxib decreased cell viability, increased apoptosis, and reduced COX-2 and MET expression.
- Neoadjuvant celecoxib significantly down-regulated COX-2 and MET expression in patient tumors compared to controls and pre-treatment levels.
Conclusions:
- This study demonstrates that selective COX-2 inhibition by celecoxib down-regulates COX-2 and MET expression in vitro and in patients with esophageal adenocarcinoma.
- These proteins are crucial for cancer progression and dissemination.
- Neoadjuvant celecoxib therapy may offer clinical benefits for esophageal adenocarcinoma patients.
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