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Devazepide (L-364718) inhibits growth and increases expression of tumor markers in HT29-S-B6 cells
M E Forgue-Lafitte1, A M Coudray, J P Aubert
1INSERM U. 55, hôpital Saint-Antoine, Paris, France.
Abstract:
Devazepide (L-364718, a non-peptide antagonist of CCK-A receptors), inhibits the proliferation and induces morphologic changes in the mucous-secreting, autonomously proliferating human cancer colon cell line (HT29-S-B6. Addition of devazepide (10 microM) for at least 3 days in the exponential phase of growth enhanced the baseline production of gastric M1 mucins 2-3-fold and that of carcinoembryonic antigens 5-fold. Moreover, devazepide induced an increase in the amount of the MUC-5AC mRNA expressed by HT29-S-B6 cells. The increased in mucins secretion induced by devazepide was persistent after removal and independent of the presence of serum. In conclusion, devazepide-L-364718 behaves as a maturation agent in the cell clone HT29-S-B6.
Insights
Devazepide, a CCK-A receptor antagonist, promotes maturation in colon cancer cells. This drug enhances mucin and carcinoembryonic antigen production, suggesting a potential therapeutic role.
Area of Science:
- Gastroenterology
- Oncology
- Molecular Biology
Background:
- Human colon cancer cell lines offer models for studying cancer progression.
- Autonomously proliferating cancer cells present therapeutic challenges.
- CCK-A receptors play roles in gastrointestinal functions and cell growth.
Purpose of the Study:
- To investigate the effects of devazepide on the human colon cancer cell line HT29-S-B6.
- To determine if devazepide influences mucin production and cell morphology.
- To explore devazepide's potential as a maturation agent in colon cancer.
Main Methods:
- Treatment of HT29-S-B6 cells with devazepide (L-364718) during exponential growth.
- Quantification of gastric M1 mucins and carcinoembryonic antigen (CEA) production.
- Analysis of MUC-5AC mRNA expression levels.
- Assessment of mucin secretion persistence and serum independence.
Main Results:
- Devazepide (10 microM) enhanced baseline production of gastric M1 mucins 2-3-fold.
- Carcinoembryonic antigen production increased 5-fold with devazepide treatment.
- Devazepide induced increased MUC-5AC mRNA expression in HT29-S-B6 cells.
- Enhanced mucin secretion was persistent and serum-independent after devazepide removal.
Conclusions:
- Devazepide acts as a maturation agent in the HT29-S-B6 colon cancer cell clone.
- The drug promotes differentiation-associated markers like mucins and CEA.
- Devazepide's effects on mucin production suggest a role in modulating cancer cell phenotype.