ArticleResearch in pharmaceutical sciences2025
Genistein potentiated the cytotoxic effect of entinostat in colorectal cancer cell lines.
Article in Research in pharmaceutical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Epigallocatechin gallate enhances panobinostat-induced cytotoxicity through HDAC modulation in colorectal cancer cells.Molecular biology reports · 2026Article
- Epigenetic regulation of the β-catenin pathway in cadmium-induced colorectal cancer progression and chemoresistance.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and purpose: Colorectal cancer (CRC) is the second leading cause of cancer death. While surgery and medicines offer complete treatment, recurrence and medication resistance pose challenges. This study assessed the cytotoxic impact of entinostat, a histone deacetylase (HDAC) inhibitor, and genistein, a soybean isoflavone, combination on CRC cells. Experimental approach: The cytotoxic effect of genistein, combined with entinostat, was tested in HCT-116 and HT-29 cell lines, along with their impact on migration and colony formation. Gene expression of the cell cycle regulatory protein CDC25A was assessed using qPCR. Findings/Results: The IC50 values of genistein, entinostat, and their combination in HCT-116 cells were 24.48 μM, 13.65 μM, and 14.55 μM, respectively. In HT-29, the IC50 values were 30.41 μM, 20.25 μM, and 19.98 μM, respectively. In the HT-29 cell line, a 1:1 ratio of entinostat and genistein resulted in a combination index of 0.6 using a concentration of 1.56 μM of each compound, indicating a synergistic effect. In contrast, no synergistic effect was produced between the two drugs in the HCT-116 cell line. In HCT-116 cells, genistein, entinostat, and their combination significantly reduced wound closure compared to the control. In contrast, in HT-29 cells, only the combination treatment was effective, while genistein and entinostat alone showed no notable impact. In HCT-116, entinostat, genistein, and their combination reduced the number of colonies significantly compared to the control, while in HT-29, only entinostat and the combination reduced the number of colonies significantly compared to the control. Furthermore, the combination of genistein with entinostat was more effective in reducing CDC25A expression in the HT-29 cells compared to entinostat treatment alone. Conclusions and implications: Combining genistein with entinostat could potentiate the entinostat cytotoxic effect in CRC.
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