Iranian journal of basic medical sciences · 2026
Combined effects of EGCG and retinol on viability and apoptosis-related gene expression in Caco-2 and HCT-116 colon cancer cells.
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Ghorbani Saeedeh, Chamani Jamshidkhan, Movahedi Monireh, Kianmehr Zahra
Аннотация
OBJECTIVES: Colorectal cancer remains a leading cause of cancer-related deaths worldwide, emphasizing the need for novel therapeutic strategies. Epigallocatechin-3-gallate (EGCG), a major green tea polyphenol, and retinol, a vitamin A derivative with antioxidant properties, have shown anti-cancer activity individually. This study investigates the combined effects of EGCG and retinol on human colorectal cancer cell lines, Caco-2 and HCT-116.
MATERIALS AND METHODS: Cytotoxic effects of EGCG and retinol, alone and in combination, were evaluated using resazurin-based cell viability assays. Intracellular reactive oxygen species (ROS) levels were measured by DCFDA assay to assess antioxidant activity. Changes in expression of apoptosis- and survival-related genes (p53, p21, AKT, and NF-κB) were analyzed using quantitative real-time PCR (RT-qPCR).
RESULTS: Combined treatment with EGCG and retinol reduced cell viability and intracellular ROS levels in both Caco-2 and HCT-116 cells. This treatment also modulated gene expression by increasing pro-apoptotic markers (p53 and p21) and decreasing anti-apoptotic markers (AKT and NF-κB), suggesting enhanced regulation of apoptosis-related pathways and inhibition of survival signaling.
CONCLUSION: The combined effects of EGCG and retinol result in enhanced cytotoxicity, antioxidant activity, and modulation of apoptosis- and survival-related genes in colorectal cancer cells, supporting their potential as a combined therapeutic approach. Further studies are required to confirm these findings and explore clinical relevance.
MATERIALS AND METHODS: Cytotoxic effects of EGCG and retinol, alone and in combination, were evaluated using resazurin-based cell viability assays. Intracellular reactive oxygen species (ROS) levels were measured by DCFDA assay to assess antioxidant activity. Changes in expression of apoptosis- and survival-related genes (p53, p21, AKT, and NF-κB) were analyzed using quantitative real-time PCR (RT-qPCR).
RESULTS: Combined treatment with EGCG and retinol reduced cell viability and intracellular ROS levels in both Caco-2 and HCT-116 cells. This treatment also modulated gene expression by increasing pro-apoptotic markers (p53 and p21) and decreasing anti-apoptotic markers (AKT and NF-κB), suggesting enhanced regulation of apoptosis-related pathways and inhibition of survival signaling.
CONCLUSION: The combined effects of EGCG and retinol result in enhanced cytotoxicity, antioxidant activity, and modulation of apoptosis- and survival-related genes in colorectal cancer cells, supporting their potential as a combined therapeutic approach. Further studies are required to confirm these findings and explore clinical relevance.