Molecular biology reports · 2026
Epigallocatechin gallate enhances panobinostat-induced cytotoxicity through HDAC modulation in colorectal cancer cells.
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Khader Mai Kamal, Abbas Manal A, Al-Kabariti Aya Y
Аннотация
PURPOSE: Colorectal cancer (CRC) is a major cause of cancer-related death due to recurrence and therapeutic resistance. This study evaluates whether combining panobinostat, a histone deacetylase (HDAC) inhibitor, with epigallocatechin gallate (EGCG), a green tea-derived polyphenol, enhances anti-tumor activity through modulation of HDAC expression in CRC cell lines.
METHODS: Cytotoxicity and migration were assessed in HCT-116 and HT-29 cells. Combination studies were performed using sub-cytotoxic concentrations (less than IC₂₅), and HDAC1, HDAC2, and HDAC4 expression levels were quantified by qPCR.
RESULTS: The combination of panobinostat and EGCG produced synergistic cytotoxic effects at low, sub-cytotoxic doses. Compared with single-agent treatment, co-treatment enhanced the cytotoxic activity of panobinostat. In HT-29 cells, EGCG inhibited migration, while 5 nM panobinostat alone showed minimal effect. Higher panobinostat doses (10 nM) and certain combination treatments significantly reduced migration. In HCT-116 cells, migration responses were limited, although selected combinations produced significant inhibition at 72 h. Mechanistically, EGCG downregulated HDAC1 in HT-29 cells and HDAC2 and HDAC4 in HCT-116 cells. In contrast, panobinostat and combination treatments upregulated HDAC expression, suggesting compensatory transcriptional feedback in response to HDAC inhibition.
CONCLUSION: Panobinostat combined with EGCG exerts synergistic cytotoxic effects in CRC, accompanied by time-and cell line-specific inhibition of cell migration and modulation of HDAC expression.
METHODS: Cytotoxicity and migration were assessed in HCT-116 and HT-29 cells. Combination studies were performed using sub-cytotoxic concentrations (less than IC₂₅), and HDAC1, HDAC2, and HDAC4 expression levels were quantified by qPCR.
RESULTS: The combination of panobinostat and EGCG produced synergistic cytotoxic effects at low, sub-cytotoxic doses. Compared with single-agent treatment, co-treatment enhanced the cytotoxic activity of panobinostat. In HT-29 cells, EGCG inhibited migration, while 5 nM panobinostat alone showed minimal effect. Higher panobinostat doses (10 nM) and certain combination treatments significantly reduced migration. In HCT-116 cells, migration responses were limited, although selected combinations produced significant inhibition at 72 h. Mechanistically, EGCG downregulated HDAC1 in HT-29 cells and HDAC2 and HDAC4 in HCT-116 cells. In contrast, panobinostat and combination treatments upregulated HDAC expression, suggesting compensatory transcriptional feedback in response to HDAC inhibition.
CONCLUSION: Panobinostat combined with EGCG exerts synergistic cytotoxic effects in CRC, accompanied by time-and cell line-specific inhibition of cell migration and modulation of HDAC expression.