Aspirin Effects on Endometrial Cancer Cell Growth
| Autor: | William S. Roberts, Jeanne L. Becker, Hector Arango, Suzane Icely, Denis Cavanagh |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
medicine.medical_specialty
Population Apoptosis Flow cytometry Andrology chemistry.chemical_compound Internal medicine In Situ Nick-End Labeling Tumor Cells Cultured medicine Humans education Aspirin education.field_of_study Dose-Response Relationship Drug medicine.diagnostic_test Cell growth business.industry Anti-Inflammatory Agents Non-Steroidal Obstetrics and Gynecology Flow Cytometry In vitro Endometrial Neoplasms Dose–response relationship Endocrinology Proto-Oncogene Proteins c-bcl-2 chemistry Female Growth inhibition business Cell Division medicine.drug |
| Zdroj: | Obstetrics & Gynecology. 97:423-427 |
| ISSN: | 0029-7844 |
| DOI: | 10.1097/00006250-200103000-00019 |
| Popis: | Objective: To find whether aspirin (acetylsalicylic acid, ASA) inhibits the growth of endometrial cancer cells in vitro in a way similar to that in colorectal cancer cells and to investigate the mechanisms by which aspirin might lead to growth inhibition. Methods: Ishikawa human endometrial tumor cells were grown in the presence of ASA (1–5 mM) for 96 hours. Controls were treated with vehicle (absolute ethanol). Cell proliferation was assessed by 3-(4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide assay. Apoptosis was determined by terminal deoxynucleotidyl transferase–mediated dUTP nick-end labeling assay. Analysis of cell-cycle distribution and bcl-2 expression was assessed by flow cytometry. Results: Acetylsalicylic acid induced a dose-dependent inhibition of Ishikawa cells in vitro. The percentage of growth inhibition was 21–88% at concentrations of 1–5 mM. It also induced apoptosis and reduced bcl-2 expression in Ishikawa cells in a dose-dependent manner. Control cells and cells treated with the lowest concentration of ASA exhibited 2% apoptosis and more than 60% of the population expressed bcl-2. Apoptosis levels increased as levels of ASA increased from 2 to 5 mM (7–58%) with a concommitant decrease in bcl-2 expression from 46% at 2 mM to 2% at 5 mM. Acetylsalicylic acid concentrations of 3 mM or greater induced a shift from the resting phase (G0/G1) to S phase of the cell cycle. Conclusion: Acetylsalicylic acid inhibited Ishikawa cell growth in vitro in a dose-dependent manner. Apoptosis is one of the mechanisms involved in the response, which can be mediated in part by downregulation of bcl-2. |
| Databáze: | OpenAIRE |
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