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Gamma Tocopherol and Lovastatin Additively Induced Apoptosis in Human Colorectal Carcinoma Cell Line (HT29)
BACKGROUND: Programmed cell death (apoptosis) is a physiological process needed to remove unwanted or damaged cells. It has been hypothesized that any failure of programmed cell death leads to the development of neoplasm. Identifying new agents which induce apoptosis in tumor cells is of great signi...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
DocS
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3941870/ https://www.ncbi.nlm.nih.gov/pubmed/24624174 |
Sumario: | BACKGROUND: Programmed cell death (apoptosis) is a physiological process needed to remove unwanted or damaged cells. It has been hypothesized that any failure of programmed cell death leads to the development of neoplasm. Identifying new agents which induce apoptosis in tumor cells is of great significance in treatment of neoplasms. Numerous studies suggest that exposure of tumor cells to statins and gamma tocopherol can lead to cell death. OBJECTIVES: The aim of this study was to evaluate the cell death induced by gamma tocopherol and lovastatin in human colorectal carcinoma cell line (HT29) using flow cytometry. MATERIAL AND METHODS: HT29 cells were grown in DMEM medium, exposed to different concentrations of lovastatin (10,20,40,100μM ) and gamma tocopherol (25,50,100,200μM) for 48 and 72 hours, individually and in combination (100μM both, 48 h). Phenotype of apoptosis was determined by means of flow cytometry. RESULTS: All Concentrations of lovastatin (10, 20, 40, 100 μM) and gamma tocopherol (25, 50, 100, 200 μM) induced an apoptotic response in HT29 cells. In combination, a significant increase in apoptosis phenotype was also demonstrated (P < 0.05). CONCLUSIONS: This study showed that lovastatin when combined with gamma tocopherol, could induce apoptosis in HT29 cells more potently than each agent alone, which uncovers the significance of targeting the proliferative signaling in different points of the pathway. |
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